Brain prosthetic restores learning capability in rats

September, 2011

Effective patterns of neural activity replayed via an artificial device inserted in the hippocampus restores lost learning capability and even improves learning in normal rats.

In the experiment, rats learned which lever to press to receive water, where the correct lever depended on which lever they had pressed previously (the levers were retractable; there was a variable delay between the first and second presentation of the levers). Microelectrodes in the rats’ brains provided data that enabled researchers to work out the firing patterns of neurons in CA1 that resulted from particular firing patterns in CA3 (previous research had established that long-term memory involves CA3 outputs being received in CA1).

Normal neural communication between these two subregions of the hippocampus was then chemically inhibited. While the rats still remembered the general rule, and still remembered that pressing the levers would gain them water, they could only remember which lever they had pressed for 5-10 seconds.

An artificial hippocampal system that could reproduce effective firing patterns (established in earlier training) was then implanted in the rats’ brains and long-term memory function was restored. Furthermore, when the ‘memory prosthetic’ was implanted in animals whose hippocampus was functioning normally, their memory improved.

The findings open up amazing possibilities for ameliorating brain damage. There is of course the greatly limiting factor that effective memory traces (spatiotemporal firing patterns) need to be recorded for each activity. This will be particularly problematic for individuals with significant damage. Perhaps one day we will all ‘record’ ourselves as a matter of course, in the same way that we might put by blood or genetic material ‘in case’! Still, it’s an exciting development.

The next step will be to repeat these results in monkeys.




tags memworks: 

tags problems: 


Older news items (pre-2010) brought over from the old website

Review supports mild memory impairment in pregnancy

A review of 14 studies testing the memory performances of more than 1,000 pregnant women, mothers and non-pregnant women, has found that pregnant women performed significantly worse on some, but not all aspects of the test. The hardest tests for the pregnant women were those that involved new or demanding tasks. Regular, well-practiced memory tasks were unlikely to be affected. The impairment wasn’t large — comparable to the modest deficits you'd find when comparing healthy 20-year-olds with healthy 60-year-olds. However, the impairment was sometimes still evident a year after birth (none looked beyond that point).

[876] Henry, J. D., & Rendell P. G.
(2007).  A review of the impact of pregnancy on memory function.
Journal of Clinical and Experimental Neuropsychology. 29(8), 793 - 793.

Effect of pregnancy on cognition depends on fetal gender

An intriguing new study may shed light on the conflicting results reported regarding the effect of pregnancy on cognition. The study, which tracked women throughout pregnancy through to postnatal resumption of menstruation, found that there was a significant effect of the sex of the baby on working memory and spatial ability. Women pregnant with boys consistently outperformed women pregnant with girls on these tests.

[1187] Vanston, C. M., & Watson N. V.
(2005).  Selective and persistent effect of foetal sex on cognition in pregnant women.
Neuroreport. 16(7), 779 - 782.

No support for idea that pregnancy affects memory and concentration

A study of pregnant women found many agreed with the popular view that pregnancy affects your memory. However, mental tests during pregnancy and after the birth found no difference between the performance of women who were pregnant and those who were not. It was possible that the affects are too mild to be picked up by the tests, or that the fatigue commonly experienced by women during pregnancy and early motherhood leads women to believe that their memory and concentration are affected.

The research was presented at the British Psychological Society annual conference in Bournemouth.

Sleep deprivation

Older news items (pre-2010) brought over from the old website

Sleep apnea therapy improves golf game

A study involving 24 golfers with diagnosed moderate to severe obstructive sleep apnea (OSA) has found that the 12 who received nasal positive airway pressure (NPAP) for their disorder not only improved their daytime sleepiness scores, but lowered their golf handicap by as much as three strokes. It is assumed this is because of improvements in cognitive function. The effect was greatest for the best golfers (those with a handicap lower than 12), even though these were often older. The findings may help improve compliance — a big issue in NPAP therapy — in golfers.

The study was presented at CHEST 2009, the 75th annual international scientific assembly of the American College of Chest Physicians (ACCP).

Alcoholism's effect on sleep persists

A study involving 42 long-term alcoholics who had not had a drink for up to 719 days (mean age 49 years, 27 men) has found that, compared to controls, alcoholics had significantly poorer sleep quality, measured by a significantly lower percentage of slow wave sleep and significantly more stage 1 non-rapid eye movement (NREM) sleep. Moreover, estimated lifetime alcohol consumption was significantly related to the scores on the Pittsburgh Sleep Quality Index, with higher lifetime consumption predicting less sleep satisfaction. The reduction in slow wave activity was specific to NREM sleep. This could act as an exacerbating factor in alcoholics' cognitive decline.

[792] Colrain, I. M., Turlington S., & Baker F. C.
(2009).  Impact of alcoholism on sleep architecture and EEG power spectra in men and women.
Sleep. 32(10), 1341 - 1352.

Why sleep deprivation causes cognitive impairment, and how to fix it

A mouse study has found a molecular pathway in the brain that is the cause of cognitive impairment due to sleep deprivation, and points to a way of preventing the cognitive deficits caused by sleep deprivation. The study showed that mice deprived of sleep had increased levels of the enzyme phosphodiesterase 4 (PDE4) and reduced levels of cAMP, crucial in forming new synaptic connections in the hippocampus. Treatment with phosphodiesterase inhibitors rescued the sleep deprivation-induced deficits in cAMP signaling, synaptic plasticity and hippocampus-dependent memory, counteracting some of the memory consequences of sleep deprivation.

[1485] Vecsey, C. G., Baillie G. S., Jaganath D., Havekes R., Daniels A., Wimmer M., et al.
(2009).  Sleep deprivation impairs cAMP signalling in the hippocampus.
Nature. 461(7267), 1122 - 1125.

Poor sleep linked to later development of Alzheimer's

A mouse study has found that amyloid-beta significantly increases during periods of sleep deprivation. The discovery follows observation that peptide levels in both mice and humans increase significantly during the day and drop at night. When mice were only allowed to sleep four hours a day for 21 days, they had higher amyloid-beta plaque build-up in their brain than similar-aged mice with regular sleeping habits. The circadian fluctuation was found to reflect the activity of orexin, a hormone that regulates wakefulness. The findings suggest insomnia, late-night habits, and irregular sleep schedules during mid-life may be linked to the later development of Alzheimer's disease.

Kang, J-E. et al. 2009. Amyloid- Dynamics Are Regulated by Orexin and the Sleep-Wake Cycle. Science, Published Online September 24

Insomniacs have to work harder

A study of 12 people with chronic primary insomnia (average age 39.4 years), and nine good sleepers, has found that the insomniacs increased brain activation relative to good sleepers during the working memory task, particularly in areas responsible for visual-spatial attention and coordination of cognitive processes. This activation may explain how PIs maintain performance on the task despite their sleep difficulties. PIs also were found to have decreased activation in visual and motor areas, which may suggest that PIs have higher baseline activation in these regions relative to good sleepers.
By the way, insomniacs might like to know that a recent study found 81% of 118 chronic insomniacs reported improved sleep after completing a five-week online cognitive behavioural therapy program, including 35% who rated themselves as much or very much improved (see

Orff, H.J. et al. 2009. Insomnia Patients Show Increased Cerebral Activation when Compared to Good Sleepers during an NBack Working Memory Task. Presented on June 9 at SLEEP 2009, the 23rd Annual Meeting of the Associated Professional Sleep Societies; Abstract ID: 0779.

Older adults less affected by sleep deprivation than younger adults

A study involving 33 older adults (59-82) and 27 younger adults (19-38) has found that while the younger adults all showed significance deterioration on three different cognitive tasks after 36 hours of sleep deprivation, the older adults did not. The finding may be due to only the healthiest older adults being chosen, suggesting that older adults who remain the healthiest late in life may be less vulnerable to a variety of stressors, not just sleep loss.
It’s worth noting that sleep deprivation affects some people more than others. A recent study has found that those with the short variant of the PERIOD3 (PER3) gene compensate for sleep loss by "recruiting" extra brain structures to help with cognitive tasks. Those with the long variant however, showed reduced activity in brain structures normally activated by the task. These participants also showed reduced brain activity in the right posterior inferior frontal gyrus after a normal waking day, a finding consistent with previous research suggesting that people with the long gene variant perform better on executive tasks earlier, but not later, in the day (see

Wang, R.L. et al. 2009. Older Adults are Less Vulnerable to Sleep Deprivation than Younger Adults during Cognitive Performance. Presented on June 10 at SLEEP 2009, the 23rd Annual Meeting of the Associated Professional Sleep Societies; Abstract ID: 0420.

Childhood sleep problems persisting through adolescence may affect cognitive abilities

A longitudinal study involving 916 twins whose parents reported their children's sleep problems from age 4 until 16, of whom 568 completed tests of executive functioning at 17, indicates that those whose sleep problems persisted through adolescence had poorer executive functioning at age 17 than children whose problems decreased to a greater extent. Sleep problems as early as age 9, but particularly around age 13, showed significant associations with later executive functions. Some problems appear to be more important than others: changes in levels of 'sleeping more than other children' and 'being overtired' were most important, and nightmares and 'trouble sleeping' the least. However, a child's level of sleep problems early in life don’t appear to be an important factor.

[930] Friedman, N. P., Corley R. P., Hewitt J. K., & Wright K. P.
(2009).  Individual Differences in Childhood Sleep Problems Predict Later Cognitive Executive Control.
Sleep. 32(3), 323 - 333.

Treating sleep apnea in Alzheimer's patients helps cognition

A study of 52 men and women with mild to moderate Alzheimer's disease and obstructive sleep apnea (OSA) has found significant improvement in patients' neurological test scores after continuous positive airway pressure (CPAP) treatment. CPAP also reduced daytime sleepiness, a common complaint of Alzheimer's patients and their caregivers. The prevalence of OSA in patients with dementia has been estimated to be as high as 70 to 80%.

Ancoli-Israel, S. et al. 2008. Cognitive Effects of Treating Obstructive Sleep Apnea in Alzheimer's Disease: A Randomized Controlled Study. Journal of the American Geriatrics Society, 56 (11), 2076-2081.

Landmark study links sleep, memory problems in elderly African-Americans

A study of older African-Americans (aged 65-90) has found that those who have trouble falling asleep are at higher risk of having memory problems, most particularly in short-term and working memory.

[242] Gamaldo, A. A., Allaire J. C., & Whitfield K. E.
(2008).  The Relationship Between Reported Problems Falling Asleep and Cognition Among African American Elderly.
Research on Aging. 30(6), 752 - 767.

One sleepless night increases dopamine

A study has found that sleep deprivation increases the level of the hormone dopamine in two brain structures: the striatum, which is involved in motivation and reward, and the thalamus, which is involved in alertness. The rise in dopamine following sleep deprivation may promote wakefulness to compensate for sleep loss. However, since the amount of dopamine correlated with feelings of fatigue and impaired performance on cognitive tasks, it appears that the adaptation is not sufficient to overcome the cognitive deterioration induced by sleep deprivation and may even contribute to it. Amphetamines increase dopamine levels.

[483] Thanos, P. K., Ferre S., Jayne M., Volkow N. D., Wang G-J., Telang F., et al.
(2008).  Sleep Deprivation Decreases Binding of [11C]Raclopride to Dopamine D2/D3 Receptors in the Human Brain.
J. Neurosci.. 28(34), 8454 - 8461.

Memory loss linked to sleep apnea

Sleep apnea occurs when a blocked airway repeatedly halts the sleeper's breathing, resulting in loud bursts of snoring and chronic daytime fatigue. Memory loss and difficulty focusing are also common complaints. While sleep loss is a common cause for such impairment, memory problems continue despite treatment for the sleep disorder, implying a long-lasting brain injury. Now a new imaging study has found significant tissue loss in brain regions that help store memory (mammillary bodies). It’s hypothesized that repeated drops in oxygen might be the cause, but further research is needed.

[958] Kumar, R., Birrer B. V. X., Macey P. M., Woo M. A., Gupta R. K., Yan-Go F. L., et al.
(2008).  Reduced mammillary body volume in patients with obstructive sleep apnea.
Neuroscience Letters. 438(3), 330 - 334.

More sleep improves cognition in Alzheimer patients with OSA

A study involving 52 participants with an average age of 77.8 years who had Alzheimer disease and obstructive sleep apnea (OSA) has found that it was increases in total sleep time in those given continuous positive airway pressure treatment that was associated with improvements in cognition, rather than improvement in oxygen levels. This suggests that the cognitive dysfunction associated with OSA in patients with dementia may be in part an effect of short sleep time.

The findings were presented at SLEEP 2008, the 22nd Annual Meeting of the Associated Professional Sleep Societies (APSS).

Green tea compounds beat OSA-related brain deficits

A study has found that rats intermittently deprived of oxygen during 12-hour “night” cycles, mimicking the experience of humans with obstructive sleep apnea, performed significantly better on a spatial memory task if they’d been treated with the polyphenols in green tea (administered through drinking water) than if they didn’t receive such chemicals. Their brains also showed less oxidative stress.

[464] Burckhardt, I. C., Gozal D., Dayyat E., Cheng Y., Li R. C., Goldbart A. D., et al.
(2008).  Green tea catechin polyphenols attenuate behavioral and oxidative responses to intermittent hypoxia.
American Journal of Respiratory and Critical Care Medicine. 177(10), 1135 - 1141.

REM sleep deprivation reduces neurogenesis

And in another sleep study, rats deprived of REM sleep for four days showed reduced cell proliferation in the dentate gyrus of the hippocampus, where most adult neurogenesis takes place. The finding indicates that REM sleep is important for brain plasticity.

[507] Guzman-Marin, R., Suntsova N., Bashir T., Nienhuis R., Szymusiak R., & McGinty D.
(2008).  Rapid eye movement sleep deprivation contributes to reduction of neurogenesis in the hippocampal dentate gyrus of the adult rat.
Sleep. 31(2), 167 - 175.

Insufficient sleep in early childhood associated with developmental delay

A long-term study of nearly 1500 young children (from 5 months to six years) found four sleep duration patterns; 6% slept less than 10 hours per night throughout early childhood, and 4.8% did so until around 41 months, when it increased. Short sleep duration was found to significantly increase the risk of low performance on the Peabody Picture Vocabulary Test–Revised (given at 5 years), suggesting that language acquisition and the consolidation of new words into memory could be significantly impeded by chronically shortened sleep duration throughout childhood. An increased risk of poorer performance on the Block Design subtest (given at 6 years) was also evident even among those who had increased their sleep duration, suggesting that there is a critical period in early childhood where the lack of sleep is particularly detrimental on various aspects of development even if the sleep duration normalizes later on.

[244] Touchette, É., Petit D., Séguin J. R., Boivin M., Tremblay R. E., & Montplaisir J. Y.
(2007).  Associations Between Sleep Duration Patterns and Behavioral/Cognitive Functioning at School Entry.
Sleep. 30(9), 1213 - 1219.

Memory problems and sleep disturbance linked in older women

A large long-running study, involving older women (average age 69) found that the nearly 25% of women who experienced cognitive decline over the 15 year period were twice as likely as women without memory problems to experience sleep disturbances, specifically problems staying asleep, and also problems falling asleep and being awake for more than 90 minutes during their sleep cycle. Women who declined on one of the two cognitive tests were also nearly twice as likely to nap more than two hours a day. However, cognitive decline was not associated with total sleep time. The association between sleep disturbances and poor cognitive function is of course well-known, but these findings raise the possibility that cognitive decline may increase the risk of sleep problems, rather than vice versa.

[679] Yaffe, K., Blackwell T., Barnes D. E., Ancoli-Israel S., Stone K. L., & For the Study of Osteoporotic Fractures Group
(2007).  Preclinical cognitive decline and subsequent sleep disturbance in older women.
Neurology. 69(3), 237 - 242.

African-American and poor children more affected by sleep problems

A study involving 166 8- and 9-year-old African-American and European-American children from varying socioeconomic backgrounds has found that sleep disruption has greater effects on cognitive performance for children from lower-income homes and African-American children. When socioeconomic status was taken into consideration, African-American and European-American children's performance on cognitive tests was similar when they slept well. But when sleep was disrupted, African-American children's performance was worse. Similarly, children from lower and higher socioeconomic backgrounds performed similarly on tests when they slept well and their sleep schedules were consistent. But when their sleep was disrupted, children from higher-income homes did better than children from lower-income homes.

[1061] Buckhalt, J. A., El-Sheikh M., & Keller P.
(2007).  Children's sleep and cognitive functioning: race and socioeconomic status as moderators of effects.
Child Development. 78(1), 213 - 231.

Sleep deprivation affects neurogenesis

A rat study has found that rats deprived of sleep for 72 hours had higher levels of the stress hormone corticosterone, and produced significantly fewer new brain cells in a particular region of the hippocampus. Preventing corticosterone levels from rising also prevented the reduction in neurogenesis.

[642] Mirescu, C., Peters J. D., Noiman L., & Gould E.
(2006).  Sleep deprivation inhibits adult neurogenesis in the hippocampus by elevating glucocorticoids.
Proceedings of the National Academy of Sciences. 103(50), 19170 - 19175.

Memory improves after sleep apnea therapy

Patients with obstructive sleep apnea (OSA) often complain of forgetfulness. A study of 58 memory-impaired patients with clinically diagnosed OSA has found that 68% of those who used continuous positive airway pressure (CPAP) machines for an average of more than 6 hours a night regained normal memory after three months. Memory improvement varied based on CPAP adherence: 21% of poor users (fewer than 2 hours/night of CPAP use), 44% of moderate users (2 to 6 hours/night) demonstrated normal memory performance after three months. However, evidence suggests this optimal level of CPAP adherence is uncommon following 3 months of treatment.

[151] Zimmerman, M. E., Arnedt T. J., Stanchina M., Millman R. P., & Aloia M. S.
(2006).  Normalization of Memory Performance and Positive Airway Pressure Adherence in Memory-Impaired Patients With Obstructive Sleep Apnea*.
Chest. 130(6), 1772 - 1778.

Childhood sleep apnea linked to brain damage, lower IQ

It’s long been known that sleep apnea, characterized by fragmented sleep, interrupted breathing and oxygen deprivation, harms children's learning ability and school performance. Now a new study involving 19 children with severe obstructive sleep apnea has identified damage in the hippocampus and the right frontal cortex, and linked that to observable deficits in performance on cognitive tests. Children with OSA had an average IQ of 85 compared to 101 in matched controls. They also performed worse on standardized tests measuring executive functions, such as verbal working memory (8 versus 15) and word fluency (9.7 versus 12). Obstructive sleep apnea affects 2% of children in the United States, but it is unclear how many of these suffer from severe apnea.

[1442] Halbower, A. C., Degaonkar M., Barker P. B., Earley C. J., Marcus C. L., Smith P. L., et al.
(2006).  Childhood Obstructive Sleep Apnea Associates with Neuropsychological Deficits and Neuronal Brain Injury.
PLoS Med. 3(8), e301 - e301.

Full text available at

Morning grogginess worse for cognition than sleep deprivation

People who awaken after eight hours of sound sleep have more impaired thinking and memory skills than they do after being deprived of sleep for more than 24 hours. The impairment is worst in the first three minutes, and the most severe effects have generally dissipated by ten minutes, but measurable effects can last up to two hours. This is consistent with reports indicating that cortical areas like the prefrontal cortex take longer to come “online” after sleep than other parts of the brain. The findings have implications for medical, safety and transportation workers who are often called upon to perform critical tasks immediately after waking, as well as for anyone abruptly woken to face an emergency situation.

Wertz, A.T., Ronda, J.M., Czeisler, C.A. & Wright, K.P.Jr. 2006. Effects of Sleep Inertia on Cognition. Journal of the American Medical Association, 295,163-164.

Losing sleep inhibits neurogenesis

A new sleep study using rats restricted rather than deprived them of sleep, to mimic more closely the normal human experience. The study found that the sleep-restricted rats had a harder time remembering a path through a maze compared to their rested counterparts. The sleep-restricted rats showed reduced survival rate of new hippocampus cells — learning spatial tasks increases the production of new cells in the hippocampus. This study shows that sleep plays a part in helping those new brain cells survive. However, the sleep-restricted rats that were forced to use visual and odor cues to remember their way through the maze did better on the task than their rested counterparts, implying that some types of learning don’t require sleep.

[994] Hairston, I. S., Little M. T. M., Scanlon M. D., Barakat M. T., Palmer T. D., Sapolsky R. M., et al.
(2005).  Sleep Restriction Suppresses Neurogenesis Induced by Hippocampus-Dependent Learning.
J Neurophysiol. 94(6), 4224 - 4233.

Breathing problems during sleep may affect mental development in infants and young children

Two new studies have found evidence that children who have problems breathing during sleep tend to score lower on tests of mental development and intelligence than do other children their age. The first study found that at one year of age, infants who have multiple, brief breathing pauses (apnea) or slow heart rates during sleep scored lower on mental development tests than did other infants of the same age. The second study found that 5-year-old children who had frequent snoring, loud or noisy breathing during sleep, or sleep apneas observed by parents scored lower standard tests measuring executive function (attention and planning), memory, and general intelligence. More than 10 percent of young children have habitual snoring, the mildest form of sleep-disordered breathing (SDB). The effects of poor sleep are often overlooked or misinterpreted in children -- rather than appearing sleepy, children may in fact seem to be more active or even hyperactive.

[1245] Gottlieb, D. J., Chase C., Vezina R. M., Heeren T. C., Corwin M. J., Auerbach S. H., et al.
(2004).  Sleep-disordered breathing symptoms are associated with poorer cognitive function in 5-year-old children☆.
The Journal of Pediatrics. 145(4), 458 - 464.

[470] Hufford, D., Hunt C. E., Corwin M. J., Baird T., Tinsley L. R., Palmer P., et al.
(2004).  Cardiorespiratory events detected by home memory monitoring and one-year neurodevelopmental outcome∗.
The Journal of Pediatrics. 145(4), 465 - 471.

More on effects of sleep loss and fatigue on memory and learning

Just to confirm what we all know (I hope): a study of medical residents from five U.S. academic health centers has found that sleep loss and fatigue affect learning, job performance and personal relationships. Specifically, residents reported adverse effects on their abilities to learn, either in short-term or long-term memory of material; on their motivation to learn; and on their higher-order thinking skills (cognitive abilities and complex thinking).

[1165] Papp, K. K., Stoller E. P., Sage P., Aikens J. E., Owens J., Avidan A., et al.
(2004).  The effects of sleep loss and fatigue on resident-physicians: a multi-institutional, mixed-method study.
Academic Medicine: Journal of the Association of American Medical Colleges. 79(5), 394 - 406.

Sleep deprivation affects working memory

A recent study investigated the working memory capacities of individuals who were sleep-deprived. For nine days, 7 of the 12 participants slept four hours each night, and 5 slept for eight hours. Each morning, participants completed a computer task to measure how quickly they could access a list of numbers they had been asked to memorize. The list could be one, three, or five items long. Then participants were presented with a series of single digits and asked to answer "yes" or "no" to indicate whether each digit was one they had memorized. Those who slept eight hours a night steadily increased their working memory efficiency on this task, but those who slept only four hours a night failed to show any improvement in memory efficiency. Motor skill did not change across days for either group of participants.

Casement, M.D., Mullington, J.M., Broussard, J.L., & Press, D.Z. 2003. The effects of prolonged sleep restriction on working memory performance. Paper presented at the annual meeting of the Society for Neuroscience, New Orleans, LA.

Strategies for sleep improvement

Learning to shape your brain activity for improved sleep & learning

We know that sleep quality affects cognitive performance. Now an exciting new study has showed that people can learn to control certain aspects of their brainwave rhythm in a way that increased relaxation, reduced the time taken to fall asleep, and, after doing it for two weeks, increased memory performance. The training involved ten sessions of neurofeedback training.

[433] Hoedlmoser, K., Pecherstorfer T., Gruber G., Anderer P., Doppelmayr M., Klimesch W., et al.
(2008).  Instrumental Conditioning of Human Sensorimotor Rhythm (12–15 Hz) and Its Impact on Sleep as Well as Declarative Learning.
Sleep. 31(10), 1401 - 1408.

tags lifestyle: 

Estrogen & Hormone therapy

Estrogen's effect on the brain is a complex story, one which we are only beginning to understand. We know it's important for women, but we're not sure about the details. One of the problems is that it appears to interact with stress. There are two aspects to estrogen's effects on women: normal monthly fluctuations in estrogen levels, and menopause.

It's also important to distinguish post-menopause (once you have completely stopped menstruating) from perimenopause (the years of menstrual irregularity leading up to this).

In general, the last few years of research seem to be coming to the conclusion that any cognitive problems women experience as they approach menopause is limited, both in time and in task, and depends in part on other factors. For example, those who experience many hot flashes may have poorer verbal memory, but the main cause for this may be the poorer sleep quality; those who are distressed or experience mood changes may find their memory and concentration affected for that reason.  These findings suggest the best approach to dealing with cognitive problems in perimenopause is to tackle the physical and/or emotional causes.

Post-menopause is different. Post-menopause is all about low estrogen levels, and the importance of estrogen for brain function. Nevertheless, estrogen therapy for postmenopausal women has had inconsistent results; there has even been some research suggesting it may increase the risk of later dementia. There is also some suggestion that it may not help those women who have cognitively stimulating environments, or are highly educated. And other indications that timing might be critical -- the age at which you begin hormone therapy. At the moment, we simply have too little clear evidence to warrant recommending hormone therapy for cognitive reasons (particularly in light of the possible cancer risk), or to know when it might be effective.

Excitingly, however (because there is no downside!), there is some evidence that physical exercise can counter the cognitive decline postmenopausal women may experience. There's also a study suggesting that the effect of low estrogen after menopause is not to impair cognition but simply to change it -- however, because women aren't prepared for, or understand, these changes, they perceive it as impairment. That would suggest that what is needed is an education program in how the brain changes (but first we have to understand exactly how it does change!).

Older news items (pre-2010) brought over from the old website

How does estrogen affect cognition?

Estrogen levels affect hippocampal wiring

Many studies have established the role of estrogen in female cognition. A rat study has now revealed the reason. It appears that the "wiring" in the hippocampus expands and retracts in relation to the amount of estrogen present during the estrous/menstrual cycle. The findings also suggest that “the brain's capacity for growth is well beyond anything we considered in the past”.
Routtenberg, A. 2005. Presented at the Society for Neuroscience's 35th Annual Meeting in Washington, D.C.

How estrogen affects the brain

A new study involved cultured rat neurons has revealed how estrogen affects learning and memory. It appears that, in females, estrogen can activate particular glutamate receptors within the hippocampus. Glutamate is the primary excitatory neurotransmitter in the brain, allowing for fast communication between neurons.
[271] Boulware, M. I., Weick J. P., Becklund B. R., Kuo S. P., Groth R. D., & Mermelstein P. G.
(2005).  Estradiol Activates Group I and II Metabotropic Glutamate Receptor Signaling, Leading to Opposing Influences on cAMP Response Element-Binding Protein.
J. Neurosci.. 25(20), 5066 - 5078.

Estrogen effect on memory influenced by stress

The question of whether estrogen helps memory and cognition in women has proven surprisingly difficult to answer, with studies giving conflicting results. Now it seems the answer to that confusion is: it depends. And one of the things it depends on may be the level of stress the woman is experiencing. A rat study has found that the performance of female rats in a water maze was affected by the interaction of hormone level (whether the rat was estrous or proestrous) with water temperature (a source of physical stress). Those rats with high hormone levels did better when the water was warm, while those with low hormone levels did better when the water was cold. The researchers suggest both timing and duration of stress might be factors in determining the effect of hormones on cognition.
[384] Rubinow, M. J., Arseneau L. M., Beverly L. J., & Juraska J. M.
(2004).  Effect of the Estrous Cycle on Water Maze Acquisition Depends on the Temperature of the Water..
Behavioral Neuroscience. 118(4), 863 - 868.

Estrogen combines with stress to impair memory

A rat study has found that male and female rats performed equally well on a task involving the prefrontal cortex when under no stress, and when highly stressed, both made significant memory errors. But importantly, after exposure to a moderate level of stress, females were impaired, but males were not. When investigated further, it was found that female rats only showed this sensitivity when they were in a high-estrogen phase of their estrus cycle. The estrogen effect was confirmed in a further study using female rats who had had their ovaries removed, thus enabling the researchers to compare the effects of estrogen versus a placebo. These results suggest that high levels of estrogen can act to enhance the stress response, causing greater stress-related cognitive impairments, while providing reassurance that estrogen appears to have no effect on cognitive performance under non-stressful conditions.
[746] Shansky, R. M., Glavis-Bloom C., Lerman D., McRae P., Benson C., Miller K., et al.
(2003).  Estrogen mediates sex differences in stress-induced prefrontal cortex dysfunction.
Mol Psychiatry. 9(5), 531 - 538.

Why estrogen helps memory

Estrogen has been implicated as having a role in memory in a number of studies, although findings have been mixed as to the value of HRT for improving memory in post-menopausal women. A new study helps us understand why estrogen might be helpful. The study details how nerve cells in the hippocampus "grow in complexity" when exposed to estrogen, increasing connections among the nerve cells. It may be that, without estrogen, the connections that are there might not work as efficiently in storing and recalling certain types of memories. Previous studies have shown that the ability of women to remember word lists varies during their normal monthly cycle.
[1005] Akama, K. T., & McEwen B. S.
(2003).  Estrogen Stimulates Postsynaptic Density-95 Rapid Protein Synthesis via the Akt/Protein Kinase B Pathway.
J. Neurosci.. 23(6), 2333 - 2339.
[880] Znamensky, V., Akama K. T., McEwen B. S., & Milner T. A.
(2003).  Estrogen Levels Regulate the Subcellular Distribution of Phosphorylated Akt in Hippocampal CA1 Dendrites.
J. Neurosci.. 23(6), 2340 - 2347.

Estrogen may dictate the problem-solving strategy chosen

Several studies have suggested estrogen may be beneficial for cognitive functioning in women. New research using rats suggests estrogen may be very specific in what types of learning it helps - and what types it may impair. In rats, it appeared to enhance place-learning, at the expense of response learning. It is suggested that postmenopausal women may experience a shift into a problem-solving mode more common to men. "Women may actually get better at performing a task from a different approach, but they are not used to doing it that way, so they view the change as an impairment."
[831] Korol, D. L., & Kolo L. L.
(2002).  Estrogen-induced changes in place and response learning in young adult female rats..
Behavioral Neuroscience. 116(3), 411 - 420.

Are you likely to develop cognitive problems in menopause?

Menopause transition may cause trouble learning

A four-year study of over 2,300 women, aged 42 to 52, has found evidence suggesting that during the early and late perimenopause women do not learn as well as they do during other menopause transition stages. Processing speed improved with repeated testing during premenopause, early perimenopause (menstrual irregularity but no "gaps" of 3 months), and postmenopause (no period for 12 months), but scores during late perimenopause (no period for three to 11 months) did not show the same degree of improvement. Improvements in processing speed were considerably reduced in late perimenopause, and improvement in verbal memory performance was reduced during both early and late perimenopause (and indeed almost non-existent during late perimenopause). These findings are consistent with self-reported memory difficulties — 60% of women state that they have memory problems during the menopause transition. The good news is that the effect seems to be temporary. Interestingly, although taking estrogen or progesterone hormones before menopause helped verbal memory and processing speed, taking them after the final period had a negative effect. This is consistent with other research indicating that the timing of hormone therapy is crucial to its effects.
[554] Greendale, G. A., Huang M. - H., Wight R. G., Seeman T., Luetters C., Avis N. E., et al.
(2009).  Effects of the menopause transition and hormone use on cognitive performance in midlife women.
Neurology. 72(21), 1850 - 1857.

Hot flashes underreported and linked to forgetfulness

In the first study to explore the relationship between objectively measured hot flashes in menopausal women and memory performance, it’s been found that women dramatically underreport the number of hot flashes they experience (by about 43%), and that, with a clear measure of hot flashes, an association between number of hot flashes and poor verbal memory is evident. There was no relationship between the number of hot flashes women thought they had and memory performance. The average number of objective hot flashes was 19.5 per day. Unsurprisingly, poor sleep also predicted poorer memory, but it was also affected by the number of hot flashes during the night when a woman was sleeping. The researchers recommend treating women for their vasomotor symptoms.
An extended interview as MP3 audio file is at
[1128] Maki, P. M., Drogos L. L., Rubin L. H., Banuvar S., Shulman L. P., & Geller S. E.
(2008).  Objective hot flashes are negatively related to verbal memory performance in midlife women.
Menopause (New York, N.Y.). 15(5), 848 - 856.

Memory problems at menopause

Findings from a study of 24 women approaching menopause have confirmed an earlier study involving over 800 women that found such women are no more likely than anyone else to suffer from memory retrieval problems. However, they did find that the women who complained more about problems with forgetfulness had a harder time learning or "encoding" new information, although they didn’t have actually have an impaired ability to learn new information. Although a larger study is needed to explore this link in more detail, the researchers suggest that stress and emotional upheaval may be responsible for attention failures that mean information isn’t encoded. The researchers did find that most of the women in their study had some sort of mood distress, including symptoms of depression or anxiety (note that this was not a random group, but women who were worried about their memory).
The study was reported at the annual meeting of the International Neuropsychological Society in Boston.

Since 1996, 803 African American and white women aged 40 to 55 have been tested annually for loss of brain function. Performance was compared annually for women in premenopausal, during menopause, and postmenopausal groups. Small but significant increases in performance were found over time during the premenopausal and perimenopausal phases, leading the authors to conclude that transition through menopause is not accompanied by a decline in working memory and perceptual speed.
[1201] Meyer, P. M., Powell L. H., Wilson R. S., Everson-Rose S. A., Kravitz H. M., Luborsky J. L., et al.
(2003).  A population-based longitudinal study of cognitive functioning in the menopausal transition.
Neurology. 61(6), 801 - 806.

Does estrogen help cognition?


Hormone replacement therapy may improve visual memory of postmenopausal women
A study of 10 postmenopausal women (aged 50-60) found that those taking combined estrogen-progestin hormone therapy for four weeks showed significantly increased activity in the prefrontal cortex when engaged in a visual matching task, compared with those on placebo.
[1409] Smith, Y. R., Love T., Persad C. C., Tkaczyk A., Nichols T. E., & Zubieta J-K.
(2006).  Impact of combined estradiol and norethindrone therapy on visuospatial working memory assessed by functional magnetic resonance imaging.
The Journal of Clinical Endocrinology and Metabolism. 91(11), 4476 - 4481.

Estrogen improves verbal memory in postmenopausal women

A study involving 60 postmenopausal women aged 32.8 to 64.9, found those receiving daily estrogen treatment (conjugated equine estrogens — Premarin) showed improved oral reading and verbal memory performance, compared to those receiving a placebo. This is consistent with brain imaging date indicating estrogen produces brain activations in the inferior parietal lobule, a region sensitive to phonological demands and implicated in reading.
[374] Shaywitz, S. E., Naftolin F., Zelterman D., Marchione K. E., Holahan J. M., Palter S. F., et al.
(2003).  Better oral reading and short-term memory in midlife, postmenopausal women taking estrogen.
Menopause (New York, N.Y.). 10(5), 420 - 426.

Hormone replacement therapy may have cognitive benefits for older women

A study of more than 2,000 women 65 or older, found that those who underwent hormone replacement therapy after menopause appeared to enjoy better mental functioning. Women 85 and older did especially well. The improvements were seen only in women free from dementia. However, the sample does not reflect the general population - most of the participants were Mormon, and the prohibition of alcohol and tobacco might be a significant factor.
[213] Carlson, M. C., Zandi P. P., Plassman B. L., Tschanz JA. T., Welsh-Bohmer K. A., Steffens D. C., et al.
(2001).  Hormone replacement therapy and reduced cognitive decline in older women: The Cache County Study.
Neurology. 57(12), 2210 - 2216.

The positive effects of estrogen on memory

Postmenopausal women who take estrogen and young college-aged women performed more consistently on memory tests compared with postmenopausal women not taking the hormone. Consistency differs from overall memory ability and is a relatively new area in research about the neuropsychology of aging. Consistency measures memory capability on multiple administrations of the same test or on several related tests in a short period of time.
The study involved 48 postmenopausal women (aged 60 - 80), and 16 younger women (18 - 30). The older women were divided into three groups: 16 non-hormone users, 16 estrogen-users and 16 estrogen and progesterone-users. Younger women and older women taking estrogen performed more consistently than the older women not taking the hormone, as well as having higher overall memory scores. Women taking a combination of estrogen and progesterone did not perform as consistently as the estrogen-only users. This finding suggests progesterone may block some of the beneficial effects of taking estrogen alone.
Wegesin, D.J., Friedman, D., Varughese, N. & Stern, Y. 2001. Effects of estrogen-use and aging on intraindividual variability in recognition memory. Paper presented to the annual Society for Neuroscience meeting in San Diego, US.


Combined hormone therapy doesn't boost memory

A study of 180 recently menopausal women found no effect of hormone therapy (a combination of estrogen and progesterone) on cognitive function. Previous research has indicated a positive benefit of estrogen on cognition, so it is speculated that progestin may counteract these positive effects.

[917] Maki, P. M., Gast M. J., Vieweg A. J., Burriss S. W., & Yaffe K.
(2007).  Hormone therapy in menopausal women with cognitive complaints: A randomized, double-blind trial.
Neurology. 69(13), 1322 - 1330.

Removing ovaries before menopause increases risk of cognitive impairment

A very long-running study of some 1,500 women who underwent the removal of one or both ovaries for non-cancer-related reasons, has found that women who had one or both ovaries removed before menopause were nearly two times more likely to develop cognitive problems or dementia compared to women who did not have the surgery. In addition, those women who were younger when their ovaries were removed were more likely to develop dementia than women who were older when their ovaries were removed. This finding adds to other research suggesting that there may be a critical age window for the protective effect of estrogen on the brain in women.

[1291] Rocca, W. A., Bower J. H., Maraganore D. M., Ahlskog J. E., Grossardt B. R., de Andrade M., et al.
(2007).  Increased risk of cognitive impairment or dementia in women who underwent oophorectomy before menopause.
Neurology. 69(11), 1074 - 1083.

Estrogen-alone hormone therapy could increase risk of dementia in older women

A new report from the Women's Health Initiative Memory Study suggests that older women using estrogen-alone hormone therapy could be at a slightly greater risk of developing dementia, including Alzheimer's disease (AD), than women who do not use any menopausal hormone therapy. Among 10,000 women using conjugated equine estrogens, 37 could be expected to develop dementia, compared to 25 in 10,000 women using the placebo. Previous reports from the Study found a greater risk with hormone therapy involving both estrogen plus progestin: among 10,000 women over age 65 using estrogen plus progestin there might be 45 cases of dementia compared to 22 cases in 10,000 older women on placebo.
It was also reported that beginning estrogen-alone hormone therapy after age 65 can have a small negative effect on overall cognitive abilities and that this negative effect may be greater in women with existing cognitive problems.
[871] Lewis, C. E., Masaki K., Coker L. H., for the Women's Health Initiative Memory Study, Shumaker S. A., Legault C., et al.
(2004).  Conjugated Equine Estrogens and Incidence of Probable Dementia and Mild Cognitive Impairment in Postmenopausal Women: Women's Health Initiative Memory Study.
JAMA. 291(24), 2947 - 2958.
[1309] Hays, J., Johnson K. C., Coker L. H., Dailey M., Bowen D., Rapp S. R., et al.
(2003).  Effect of Estrogen Plus Progestin on Global Cognitive Function in Postmenopausal Women: The Women's Health Initiative Memory Study: A Randomized Controlled Trial.
JAMA. 289(20), 2663 - 2672.

For women over 65, Combined Hormone Therapy increases risk of dementia

Much to the researchers’ surprise and disappointment, a four-year experiment involving 4,532 women at 39 medical centers, has found that combined hormone therapy (involving both estrogen and progestin) doubles the risk of Alzheimer's disease and other types of dementia in women who began the treatment at age 65 or older, although the risk is still small : for every 10,000 women 65 and older who take hormones, 23 of the predicted 45 cases of dementia a year, will be attributable to the hormones. The study also found that the combined hormone therapy produced no improvement in general cognitive function, and in fact had adverse effects on cognition among some women. This supports an earlier study suggesting that, while estrogen is helpful to cognitive function in postmenopausal women, the benefits can be cancelled out by progestin / progesterone. The study also confirmed previous research showing that the combination therapy increased the risk of stroke - previous research has indicated that risk factors for stroke are also risk factors for cognitive decline.
[918] Jackson, R. D., Morley Kotchen J., Wassertheil-Smoller S., Wactawski-Wende J., Shumaker S. A., Legault C., et al.
(2003).  Estrogen Plus Progestin and the Incidence of Dementia and Mild Cognitive Impairment in Postmenopausal Women: The Women's Health Initiative Memory Study: A Randomized Controlled Trial.
JAMA. 289(20), 2651 - 2662.
[1309] Hays, J., Johnson K. C., Coker L. H., Dailey M., Bowen D., Rapp S. R., et al.
(2003).  Effect of Estrogen Plus Progestin on Global Cognitive Function in Postmenopausal Women: The Women's Health Initiative Memory Study: A Randomized Controlled Trial.
JAMA. 289(20), 2663 - 2672.
[1194] Rossouw, J. E., Aragaki A., Safford M., Stein E., Laowattana S., Mysiw J. W., et al.
(2003).  Effect of Estrogen Plus Progestin on Stroke in Postmenopausal Women: The Women's Health Initiative: A Randomized Trial.
JAMA. 289(20), 2673 - 2684.

When is estrogen therapy helpful?

Cognitive benefit of estrogen minimal for the highly educated?
A mouse study sheds light on the mixed results coming from investigations into the cognitive effects of hormone replacement therapy. The study found no beneficial effect of estrogen in female mice who were raised in a stimulating environment. On the other hand, mice raised in standard conditions showed significant spatial and object memory improvement when treated with a high dose of estrogen (following removal of their ovaries). Among mice not treated with estrogen, an enriched environment alone significantly improved spatial memory. These results might help to explain why studies of hormone replacement therapy do not show beneficial effects for all women. Most studies of HRT use very well-educated women.
[1229] GRESACK, J. E., & Frick K. M.
Neuroscience. 128(3), 459 - 471.

New insights into hormone therapy highlight when estrogen best aids brain

Several studies have been exploring some of the many variables that may be important in determining the effect of hormone replacement therapy.
A mouse study compared the effects of receiving daily estrogen injections (“continuous treatment”) with the effects of receiving it every four days (“cyclical treatment”). The treatment lasted three months. Ovariectomized mice receiving the continuous treatment performed better on memory tasks than those receiving cyclical treatment.
Another mouse study compared the brains of ovariectomized mice treated with continuous estrogen for 47 days with those not so treated, and found that, after five days on estrogen, estrogen-treated mice produced more of the proteins important for neuron repair and neuronal function. However, with prolonged, continuous estrogen treatment, this effect diminished, and by day 47 the estrogen-treated mice were similar to the non-estrogen-treated mice in levels of the repair proteins. Mice that did not receive estrogen showed an elevation of a brain protein associated with the negative aspects of brain aging, while estrogen-treated mice did not.
A rat study examined the effects of progesterone (a component of many hormone therapies), and found that ovariectomized rats receiving progesterone exhibited deficiencies in learning and memory, supporting the hypothesis that progesterone negatively affects memory during aging. It’s suggested that the negative outcome of several studies evaluating combined estrogen/progesterone HT may be due, in part, to unfavorable effects of progesterone.
Other rat studies have found that two established protective actions of estrogen with relevance to Alzheimer's are negatively affected by the presence of progesterone.
Another study using neurons in culture demonstrated the importance of timing. Neurons exposed to estrogen prior to exposure to beta-amyloid (the protein implicated in Alzheimers) had a significantly greater rate of survival than those exposed to estrogen after being exposed to beta-amyloid. The results are consistent with clinical studies in which women who received estrogen hormone therapy at the time of menopause, before cognitive degeneration becomes apparent, have a lower risk of developing Alzheimer's disease than women who never receive any sort of HT, while for women in their 60s and 70s, hormone therapy may make things worse.
Papers presented at the 34th Society for Neuroscience annual meeting in San Diego in late October 2004.

Dangers of hormone therapy

Getting the benefits of estrogen without the downside

We know estrogen helps learning and memory, but estrogen therapy also increases cancer risk. That’s why the results of a mouse study are exciting. The study found that estrogen acts through calpain, a protein crucial to learning and memory, and like adrenalin (which acts like a hormone in most of the body but as a neurotransmitter in the brain), it does so as a neurotransmitter, modulating synaptic transmission. The findings suggest drugs that target calpain directly may provide the same cognitive benefits of estrogen therapy, without the medical risks.
[299] Zadran, S., Qin Q., Bi X., Zadran H., Kim Y., Foy M. R., et al.
(2009).  17-β-Estradiol increases neuronal excitability through MAP kinase-induced calpain activation.
Proceedings of the National Academy of Sciences. 106(51), 21936 - 21941.

Other aids to help memory in menopausal women

Less cognitive impairment seen in women taking raloxifene

Raloxifene modulates the activity of the hormone estrogen and is one of the most widely prescribed drugs for the treatment of osteoporosis. A 3-year worldwide clinical trial involving 7705 postmenopausal women with osteoporosis found that those taking 120mg of raloxifene had a 33% less chance of developing mild cognitive impairment. There was no cognitive benefit from a 60mg dose. Note that, of the 5386 women participating in the cognitive part of this trial, only 3.4% had mild cognitive impairment, and 1% had dementia.
[757] Yaffe, K., Krueger K., Cummings S. R., Blackwell T., Henderson V. W., Sarkar S., et al.
(2005).  Effect of Raloxifene on Prevention of Dementia and Cognitive Impairment in Older Women: The Multiple Outcomes of Raloxifene Evaluation (MORE) Randomized Trial.
Am J Psychiatry. 162(4), 683 - 690.

The estrogen drug raloxifene may help prevent cognitive decline in women over 70

The designer estrogen drug raloxifene has been prescribed to millions of postmenopausal women for osteoporosis, but its effects on the aging brain are unclear. A new study shows that although raloxifene does not affect the cognitive performance of most women, it may help prevent decline among women older than 70 and women whose cognitive performance is declining regardless of age.
Yaffe, K. et al. 2001. Cognitive Function in Postmenopausal Women Treated with Raloxifene. New England Journal of Medicine, 344, 1207-1213.Yaffe, K. et al. 2001. Cognitive Function in Postmenopausal Women Treated with Raloxifene. New England Journal of Medicine, 344, 1207-1213.

Fitness counteracts cognitive decline from hormone-replacement therapy

A study of 54 postmenopausal women (aged 58 to 80) suggests that being physically fit offsets cognitive declines attributed to long-term hormone-replacement therapy. It was found that gray matter in four regions (left and right prefrontal cortex, left parahippocampal gyrus and left subgenual cortex) was progressively reduced with longer hormone treatment, with the decline beginning after more than 10 years of treatment. Therapy shorter than 10 years was associated with increased tissue volume. Higher fitness scores were also associated with greater tissue volume. Those undergoing long-term hormone therapy had more modest declines in tissue loss if their fitness level was high. Higher fitness levels were also associated with greater prefrontal white matter regions and in the genu of the corpus callosum. The findings need to be replicated with a larger sample, but are in line with animal studies finding that estrogen and exercise have similar effects: both stimulate brain-derived neurotrophic factor.
[375] Erickson, K. I., Colcombe S. J., Elavsky S., McAuley E., Korol D. L., Scalf P. E., et al.
(2007).  Interactive effects of fitness and hormone treatment on brain health in postmenopausal women.
Neurobiology of Aging. 28(2), 179 - 185.

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Alcohol's damage to the brain

While moderate drinking seems to have a protective effect against age-related cognitive decline and dementia, cognitive impairment produced by excess alcohol is only too evident. Here are a few less obvious cognitive effects:

Simulated laparoscopic surgery was impaired in both novices and experts on the day following an evening during which excessive alcohol was consumed, although experts were less impaired than novices. Performance had returned to baseline levels by 4:00 p.m.

When people drank before viewing a video of serious road traffic accidents, those given a smaller amount of alcohol experienced more flashbacks during the next week than those given a larger amount of alcohol, and those given no alcohol. Those who had large amounts of alcohol had poorer memories of the event. It’s suggested that alcohol impairs contextual memory first.

Another study found that recognition of different-race faces was unaffected by alcohol, but recognition of own-race faces was — meaning recognition of same-race faces was at about the same level of accuracy as different-race faces.

Cognitive impairment produced by excess alcohol is of course only too evident. Here are a few less obvious cognitive effects:

Simulated laparoscopic surgery was impaired in both novices and experts on the day following an evening during which excessive alcohol was consumed, although experts were less impaired than novices. Performance had returned to baseline levels by 4:00 p.m.

When people drank before viewing a video of serious road traffic accidents, those given a smaller amount of alcohol experienced more flashbacks during the next week than those given a larger amount of alcohol, and those given no alcohol. Those who had large amounts of alcohol had poorer memories of the event. It’s suggested that alcohol impairs contextual memory first.

Another study found that recognition of different-race faces was unaffected by alcohol, but recognition of own-race faces was — meaning recognition of same-race faces was at about the same level of accuracy as different-race faces.

Heavy drinking

Heavy drinking can be chronic, or occasional. Both have their price.

A rat study suggests that it doesn’t take all that long before heavy drinking produces long-lasting cognitive deficits. Rats drinking for eight weeks (but not four) developed deficits that lasted at least 12 weeks after drinking stopped — “equivalent to a human that drank six to eight beers or one bottle of wine a day every day for six years experiencing learning and memory deficits up to nine years after they stopped drinking alcohol."

Brain scans of heavy social drinkers have revealed damage to white matter that was associated with lower executive and working memory functions. This is consistent with a self-report study that found that heavy users of alcohol were more likely to miss appointments, forget birthdays and pay bills on time, and to forget whether they had done something or where they had put something.

One study suggests that heavy drinking is particularly a problem for those infected with HIV. The mediotemporal lobe is affected early in both these conditions, so it is not surprising that those positive for HIV with a history of chronic heavy drinking were found to have trouble encoding new information for long-term memory.

Smoking and alcohol

Smoking has a particularly negative effect in conjunction with alcohol (and unfortunately they are often found in tandem). While moderate drinking can in some circumstances have positive effects on the brain, this is probably not the case for those who smoke. Moreover, smoking makes it much harder for the brain to recover from the effects of alcohol abuse, the damage done to the brain by heavy alcohol consumption is likely to be much worse if the individual is a smoker.


One of the characteristics of alcoholics is that they don’t recognize the extent of their problem. So perhaps it’s no surprise that a study found that alcoholics were relatively unaware of their memory deficits and believed that their memory was much better than it was. Moreover, the greater their deficits, the less they were aware of them!

Years of heavy alcohol consumption impair executive functions, including judgment, problem solving, decision making, planning, and social conduct.

Imaging studies indicate that the brains of alcoholics develop compensatory mechanisms to maintain cognitive skills despite alcohol's damages. It seems likely that this wider activity comes at the expense of other tasks, thus reducing their ability to multitask.

Excessive chronic drinking is also associated with deficits in comprehending emotional information, such as recognizing different facial expressions, and visuospatial deficits, characterized by difficulties completing tasks such as putting pieces of a puzzle together or map reading. While long-term abstinence can recover most of the cognitive function lost, spatial processing abilities seem much harder to recover.

In line with these problems of executive function, episodic and spatial memory, the prefrontal cortex and the hippocampus are especially vulnerable to the effects of chronic alcoholism.

Alcoholics have also been found to have an impaired cortisol response to stress, and this is associated with lower scores on measures of problem-solving ability and memory. Another exacerbating factor may come from poorer sleep — recovering alcoholics have been found to have significantly poorer sleep quality.

There is some evidence that women are more vulnerable to the effects of binge drinking and chronic heavy drinking.

Alcohol and the adolescent brain

Binge drinking is particularly evident among young people. Several studies point to effects on executive functions, including attention and working memory. This has consequences for planning and decision-making, as well as memory tasks.

Memory impairment following too much alcohol is particularly common among adolescent drinkers, possibly because of disruption in the hippocampus, which is still developing during adolescence.

Other physiological consequences of teenage binge drinking may be damaged white matter connectivity, and reduced activity of many neurotransmitter genes. There is some indication that some of these effects may persist into adulthood.

Prenatal exposure

Studies suggest that there is no safe dose, nor safe time to drink, for pregnant women, although the timing does affect the nature of the damage. It seems that alcohol is especially damaging for the development of the dopamine system.

Children prenatally exposed to alcohol are not consistently impaired however. A monkey study suggests why — it seems a gene variant makes the carrier more susceptible to the effects of fetal alcohol exposure. The gene has previously been implicated in increased depression risk.

Other research has suggested that children whose mothers are older than 30 years, those whose mothers have alcohol dependence, those whose parents provide a less stimulating environment, and those whose mothers reported drinking during the time of conception, are at greater risk from prenatal alcohol exposure.

It’s also the case that cognitive deficits are not always evident. One study found that children prenatally exposed to moderate-to-heavy levels of alcohol were perfectly competent at simple tasks, but failed when asked to multi-task. Such working memory deficits may partly be a result of slower processing speed.

Hope comes from a finding that two factors can considerably mitigate the negative effects of prenatal alcohol exposure: being diagnosed early in life and being raised in a stable and nurturing environment.

Children with fetal alcohol spectrum disorder are particularly impaired in mathematical ability, possibly due to specific deficits in memory for numbers and sequences.

Distinguishing Fetal Alcohol Spectrum Disorder from other developmental disorders may have got easier, with a simple test that measures eye movement.

Older news items (pre-2010) brought over from the old website

Alcoholism's effect on sleep persists

A study involving 42 long-term alcoholics who had not had a drink for up to 719 days (mean age 49 years, 27 men) has found that, compared to controls, alcoholics had significantly poorer sleep quality, measured by a significantly lower percentage of slow wave sleep and significantly more stage 1 non-rapid eye movement (NREM) sleep. Moreover, estimated lifetime alcohol consumption was significantly related to the scores on the Pittsburgh Sleep Quality Index, with higher lifetime consumption predicting less sleep satisfaction. The reduction in slow wave activity was specific to NREM sleep. This could act as an exacerbating factor in alcoholics' cognitive decline.

[792] Colrain, I. M., Turlington S., & Baker F. C. (2009).  Impact of alcoholism on sleep architecture and EEG power spectra in men and women. Sleep. 32(10), 1341 - 1352.

Alcoholics show abnormal brain activity when processing facial expressions

Excessive chronic drinking is known to be associated with deficits in comprehending emotional information, such as recognizing different facial expressions. Now an imaging study of abstinent long-term alcoholics has found that they show decreased and abnormal activity in the amygdala and hippocampus when looking at facial expressions. They also show increased activity in the lateral prefrontal cortex, perhaps in an attempt to compensate for the failure of the limbic areas. The finding is consistent with other studies showing alcoholics invoking additional and sometimes higher-order brain systems to accomplish a relatively simple task at normal levels. The study compared 15 abstinent long-term alcoholics and 15 healthy, nonalcoholic controls, matched on socioeconomic backgrounds, age, education, and IQ.

[1044] Marinkovic, K., Oscar-Berman M., Urban T., O'Reilly C. E., Howard J. A., Sawyer K., et al. (2009).  Alcoholism and dampened temporal limbic activation to emotional faces. Alcoholism, Clinical and Experimental Research. 33(11), 1880 - 1892.

Binge drinking affects attention and working memory in young university students

A Spanish study of 95 first-year university students, 42 of them binge drinkers, has found that those who engaged in binge drinking required greater attentional processing during a visual working memory task in order to carry it out correctly. They also had difficulties differentiating between relevant and irrelevant stimuli. Binge drinkers are defined as males who drink five or more standard alcohol drinks, and females who drink four or more, on one occasion and within a two-hour interval. Some 40% of university students in the U.S. are considered binge drinkers.

[231] Crego, A., Holguín S R., Parada M., Mota N., Corral M., & Cadaveira F.
(2009).  Binge drinking affects attentional and visual working memory processing in young university students.
Alcoholism, Clinical and Experimental Research. 33(11), 1870 - 1879.

HIV infection and chronic drinking together impair encoding of new experiences

A study involving 40 individuals with HIV, 38 with chronic alcoholism, 47 with both HIV and chronic alcoholism, and 39 controls, has found that although those with only one of these disorders mostly performed at levels comparable to controls on episodic and working memory tasks, those who were both positive for HIV and had a history of chronic heavy drinking were impaired on tests of immediate episodic memory (but not working memory) — meaning that they have trouble encoding new information for long-term memory. The finding is consistent with the fact that the mediotemporal lobe is affected early by both these conditions. Heavy drinking is very common among those infected with HIV.

[440] Fama, R., Rosenbloom M. J., Nichols N. B., Pfefferbaum A., & Sullivan E. V.
(2009).  Working and episodic memory in HIV infection, alcoholism, and their comorbidity: baseline and 1-year follow-up examinations.
Alcoholism, Clinical and Experimental Research. 33(10), 1815 - 1824.

Adolescent binge drinking may compromise white matter

An imaging study of 28 teens, of whom half had a history of binge drinking (but did not meet the criteria for alcohol abuse), has found that those who had engaged in binge drinking episodes had lower coherence of white matter fibers in 18 different areas across the brain. The findings add to a growing literature indicating that adolescent alcohol involvement is associated with specific brain characteristics. White matter integrity is essential to the efficient relay of information in the brain.

[1426] McQueeny, T., Schweinsburg B. C., Schweinsburg A. D., Jacobus J., Bava S., Frank L. R., et al.
(2009).  Altered white matter integrity in adolescent binge drinkers.
Alcoholism, Clinical and Experimental Research. 33(7), 1278 - 1285.

Alcoholics’ brains maintain language skills at a cost

Despite the damage done by alcoholism to the frontal lobes and cerebellum, areas involved in language processing, alcoholics' language skills appear to be relatively spared from alcohol's damaging effects. A new study of 12 alcoholic males and 12 healthy controls suggests that alcoholics develop compensatory mechanisms to maintain their language skills despite alcohol's damages. The comparable performance on an auditory language task between the two groups was underlain by different neural activity (specifically, the alcoholic group showed greater activity in the left middle frontal gyrus, the right superior frontal gyrus, and the cerebellar vermis). It seems likely that this wider activity comes at the expense of other tasks, thus reducing their ability to multitask.

[926] Chanraud-Guillermo, S., Andoh J., Martelli C., Artiges E., Pallier C., Aubin H. - J., et al. (2009).  Imaging of language-related brain regions in detoxified alcoholics. Alcoholism, Clinical and Experimental Research. 33(6), 977 - 984.

Drinking alcohol associated with smaller brain volume

It is estimated that brain volume decreases by 1.9% per decade, accompanied by an increase in white matter lesions. Because moderate alcohol consumption has been associated with a lower risk of cardiovascular disease, it’s been thought that small amounts of alcohol might also reduce age-related declines in brain volume, although it’s known that large amounts of alcohol will reduce brain volume. However, a large, long-running study, has now found that, even at low levels of alcohol consumption, brain volume was negatively affected. Moreover, although men were more likely to be heavier drinkers, the association between drinking and brain volume was stronger in women.

[1191] Paul, C A., Au R., Fredman L., Massaro J. M., Seshadri S., DeCarli C., et al.
(2008).  Association of Alcohol Consumption With Brain Volume in the Framingham Study.
Arch Neurol. 65(10), 1363 - 1367.

Heavy, chronic drinking can cause significant hippocampal tissue loss

An imaging study of 8 heavy-drinking alcoholics and 8 age and ethnicity matched non-alcoholics (all male) found that total hippocampus volume was significantly reduced among the alcoholics.

[677] Beresford, T. P., Arciniegas D. B., Alfers J., Clapp L., Martin B., Du Y., et al. (2006).  Hippocampus Volume Loss Due to Chronic Heavy Drinking. Alcoholism: Clinical and Experimental Research. 30(11), 1866 - 1870.

Most of the cognitive deficits associated with alcoholism recoverable

Results of a study involving middle-aged alcoholics who have been sober for six months to 13 years, suggest that long-term abstinent alcoholics can recover most of their neurocognitive deficits. However, deficits in spatial-processing abilities continued. Visuospatial processes are important for many daily activities, including driving, reading a map, assembling things, and performing tasks that require spatial orientation. The study doesn’t however know how much damage had been done when the alcoholics ceased drinking; further studies are exploring the recovery of older abstinent alcoholics who ceased drinking at different ages.

[856] Fein, G., Torres J., Price L. J., & Sclafani V. D. (2006).  Cognitive Performance in Long-Term Abstinent Alcoholic Individuals. Alcoholism: Clinical and Experimental Research. 30(9), 1538 - 1544.

Brain atrophy occurs faster in women alcoholics

A study of 34 male and 42 female alcoholics has found that, although the women had been alcoholics for just 5.5 years on average, compared to the average 10.4 years for the men, the women had lost as much proportionate brain volume as the men. The findings are consistent with other studies suggesting that women suffer from the effects of alcohol abuse faster.

[1258] Mann, K., Ackermann K., Croissant B., Mundle G., Nakovics H., & Diehl A. (2005).  Neuroimaging of Gender Differences in Alcohol Dependence: Are Women More Vulnerable?. Alcoholism: Clinical and Experimental Research. 29(5), 896 - 901.

Drinking for just eight weeks impairs learning and memory in mice

It’s well established that chronic alcohol consumption can produce deficits in learning and memory. A new rodent study, however, is the first to show that continuous drinking for as little as eight weeks can produce deficits in learning and memory that last at least 12 weeks after drinking stopped — “equivalent to a human that drank six to eight beers or one bottle of wine a day every day for six years experiencing learning and memory deficits up to nine years after they stopped drinking alcohol." These deficits were global — that is, they affected long-term memory for every type of task tested. Short-term memory was not affected. Rats who drank for only four weeks did not experience the same effects.

[522] Farr, S. A., Scherrer J. F., Banks W. A., Flood J. F., & Morley J. E.
(2005).  Chronic Ethanol Consumption Impairs Learning and Memory After Cessation of Ethanol.
Alcoholism: Clinical and Experimental Research. 29(6), 971 - 982.

Cognitive effects of binge drinking worse for women

A new study looked at the cognitive effects of binge drinking, which apparently is on the rise in several countries, including Britain and the US. The study involved 100 healthy moderate-to-heavy social drinkers aged between 18 and 30. There were equal numbers of males and females. The study found that female binge drinkers performed worse on the working-memory and vigilance tasks than did the female non-binge drinkers.

[1311] Townshend, J. M., & Duka T.
(2005).  Binge Drinking, Cognitive Performance and Mood in a Population of Young Social Drinkers.
Alcoholism: Clinical and Experimental Research. 29(3), 317 - 325.

Alcohol's damaging effects on adolescent brain function

A number of speakers at Symposium speakers at the June 2004 Research Society on Alcoholism meeting in Vancouver, reported on research concerning the vulnerability of the adolescent brain to the damaging effects of alcohol. Some of the findings presented were:

  • The adolescent brain is more vulnerable than the adult brain to disruption from activities such as binge drinking. Adolescent rats that were exposed to binge drinking appear to have permanent damage in their adult brains.
  • Subtle but important brain changes occur among adolescents with Alcohol Use Disorder, resulting in a decreased ability in problem solving, verbal and non-verbal retrieval, visuospatial skills, and working memory.
  • The association between antisocial behavior during adolescence and alcoholism may be explained by abnormalities in the frontal limbic system, which appears to cause "blunted emotional reactivity".
  • Alcohol-induced memory impairments, such as "blackouts", are particularly common among young drinkers and may be at least in part due to disrupted neural plasticity in the hippocampus, which is centrally involved in the formation of autobiographical memories.

[1238] Monti, P. M., Miranda, Jr R., Nixon K., Sher K. J., Swartzwelder S. H., Tapert S. F., et al.
(2005).  Adolescence: Booze, Brains, and Behavior.
Alcoholism: Clinical and Experimental Research. 29(2), 207 - 220.

Alcoholics can have deficits in visuoperception and frontal executive function despite sobriety

Detoxified alcoholics often have visuospatial and visuoperceptual deficits, characterized by difficulties completing tasks such as putting pieces of a puzzle together or map reading. A new study has found that, even with prolonged sobriety, alcoholics show deficits in visuoperception and frontal executive functioning of the brain. Furthermore, alcoholics utilize a more complex higher-order cognitive system (frontal executive functions) to perform the same tasks as individuals without a history of alcoholism. The potential problem with this is that if that same system is needed for a competing task, alcoholics may be at a disadvantage because that system would otherwise be engaged. The study involved 51 recently detoxified nonamnesic alcoholic men (ages 29 to 66 years) compared with 63 "normal," control men (ages 21 to 70 years).

Fama, R., Pfefferbaum, A. & Sullivan, E. V. 2004. Perceptual Learning in Detoxified Alcoholic Men: Contributions From Explicit Memory, Executive Function, and Age. Alcoholism: Clinical & Experimental Research, 28(11), 1657-1665.

New brain cells develop during alcohol abstinence

A rat study has found that the detrimental effect of alcohol on the formation of new neurons in the adult rat hippocampus is followed by a pronounced increase in new neuron formation in the hippocampus within four-to-five weeks of abstinence. This included a twofold burst in brain cell proliferation at day seven of abstinence. The findings may have significant implications for treatment of alcoholism during recovery. The discovery of regeneration of neurons in recovery opens up new avenues of therapies aimed at regeneration of brain cells.

[393] Nixon, K., & Crews F. T. (2004).  Temporally Specific Burst in Cell Proliferation Increases Hippocampal Neurogenesis in Protracted Abstinence from Alcohol. J. Neurosci.. 24(43), 9714 - 9722.

Cognitive function of alcohol abuse patients may influence treatment outcome

Years of heavy alcohol consumption are known to impair many abilities generally referred to as “executive functions.” Such functions include judgment, problem solving, decision making, planning, and social conduct. But alcohol affects executive functioning both chronically and acutely. New research has found that alcohol abuse patients show significant deficits in executive functioning (specifically, abstract reasoning, memory discrimination, and effectiveness on timed tasks) during the critical first weeks of abstinence. The finding has implications for treatment programs, as the early phases of most treatment programs for alcohol abusers commonly require working in groups, making plans for the future, inhibiting behaviors related to their addiction, and remembering specific things. It is suggested that clinicians should scale down their expectations of what patients can do until more of their executive functioning comes back. The researchers are now intending to explore how long it takes the majority of people to regain most of their executive functioning.

[194] Zinn, S., Stein R., & Swartzwelder S. H. (2004).  Executive Functioning Early in Abstinence From Alcohol. Alcoholism: Clinical and Experimental Research. 28(9), 1338 - 1346.

Brain damage found among heavy social drinkers

Almost all knowledge about brain damage due to chronic alcohol consumption has been gathered from alcoholics, generally toward the end of an institutionalized treatment program or many months into abstinence. A new study however, uses magnetic resonance technology to examine brain damage in heavy drinkers who are not in treatment and function relatively well in the community. The study found that frontal white matter NAA – generally considered to be a marker of neuronal damage – was lower in heavy drinkers than light drinkers, and was associated with lower executive and working memory functions. Some of the behaviors that could be associated with the metabolite changes include the inability to apply consequences from past actions, difficulties with abstract concepts of time and money, difficulties with storing and retrieving information, and frequently needing external motivators.

[220] Weiner, M. W., Meyerhoff D. J., Blumenfeld R., Truran D., Lindgren J., Flenniken D., et al.
(2004).  Effects of Heavy Drinking, Binge Drinking, and Family History of Alcoholism on Regional Brain Metabolites.
Alcoholism: Clinical and Experimental Research. 28(4), 650 - 661.

Even small amounts of alcohol or anesthetics may damage the developing brain

Mouse studies suggest that even small amounts of alcohol or anesthetic drugs can trigger nerve cell death in the developing brain. The brain appears most sensitive to this effect during the development stage known as the brain growth spurt. In humans this lasts from about the sixth month of pregnancy to a child's third birthday. Nerve cells are genetically programmed to commit suicide if they fail to make synaptic connections on time. Alcohol and anesthetic drugs interfere with the brain's neurotransmitter systems and with the formation of those synaptic connections, automatically activating a signal within the neuron that directs it to commit suicide.

Olney, J.W. 2004. Perinatal Drug/Alcohol Exposure and Neuronal Suicide – Public Health Implications. Paper presented February 14 at the annual meeting of the American Association for the Advancement of Science in Seattle.

Hippocampal damage seen in those with alcoholic memory disorder and those with Alzheimer's

A comparison between the brains of five men with alcoholic Korsakoff's syndrome and the brains of men with Alzheimer's disease as well as the brains of healthy men, found that the brains of all Korsakoff's patients and Alzheimer's patients were comparable in significant volume loss in the hippocampus. Greater hippocampal damage (for Korsakoff's patients) and smaller hippocampal size (for Alzheimer’s) was correlated with poorer memory performance. It is suggested that, although there are of course a number of differences between these disorders, the nature of the memory impairment may be the same. Awareness of the similarities may help detection of both disorders.

[262] Sullivan, E. V., & Marsh L. (2003).  Hippocampal volume deficits in alcoholic Korsakoff's syndrome. Neurology. 61(12), 1716 - 1719.

Alcohol damages day-to-day memory function

A new study involving 763 participants (465 female, 298 males) used self-report questionnaires: the Prospective Memory Questionnaire (PMQ), the Everyday Memory Questionnaire (EMQ), and the UEL (University of East London) Recreational Drug Use Questionnaire, and found that heavy users of alcohol reported making consistently more errors than those who said that they consumed little or no alcohol. More specifically, those who reported higher levels of alcohol consumption were more likely to miss appointments, forget birthdays and pay bills on time (prospective memory), as well as more problems remembering whether they had done something, like locking the door or switching off the lights or oven, or where they had put items like house keys. The study also found a significant increase in reported memory problems by people who claimed to drink between 10 and 25 units each week in comparison to non-drinkers – this is within the ’safe drinking’ limits suggested by U.K. government guidelines.

[1042] Ling, J., Heffernan T. M., Buchanan T., Rodgers J., Scholey A. B., & Parrott A. C.
(2003).  Effects of Alcohol on Subjective Ratings of Prospective and Everyday Memory Deficits.
Alcoholism: Clinical and Experimental Research. 27(6), 970 - 974.

Study of alcoholics reveals connection between cerebellum and prefrontal cortex

Two functions commonly compromised by chronic alcoholism are executive functions (such as problem solving, putting things in order, working memory, doing multiple tasks at once) and balance (the ability to walk a straight line or stand on one foot, especially with eyes closed or in the dark). Executive functions are primarily processed in the prefrontal cortex, while balance and postural stability are functions of the cerebellum. Previous studies have shown that the prefrontal cortex and regions of the cerebellum are especially vulnerable to the effects of chronic alcoholism. Although these areas are spatially far apart (the former in the frontal lobes, the latter in the hindbrain), they are connected in a variety of ways, most particularly through the pons and the thalamus. An imaging study of 25 nonamnesic alcoholic men suggests that these connections may compound the damaging effects of alcohol on these brain regions, and that the cerebellum, through these connections, can exert a significant effect on functions of the prefrontal cortex.

[356] Sullivan, E. V. (2003).  Compromised Pontocerebellar and Cerebellothalamocortical Systems: Speculations on Their Contributions to Cognitive and Motor Impairment in Nonamnesic Alcoholism. Alcoholism: Clinical and Experimental Research. 27(9), 1409 - 1419.

Alcoholics' cognitive impairment associated with impaired reaction to stress

The body secretes a hormone called cortisol in response to stress. Areas of the brain involved in memory and problem-solving are responsive to cortisol. A new study has found impaired release of cortisol in recently detoxified alcoholics when performing two tasks known to induce stress: mental arithmetic problems and a "cold pressor" task, which requires submerging one hand in ice water for 90 seconds. This was associated with lower scores on measures of problem-solving ability and memory. The study also found that, among alcoholics, the number of withdrawals from alcohol was the strongest predictor of memory impairments, but not of problem-solving ability. The greater the alcoholics' relative cortisol levels were during alcohol withdrawal, the more likely they were to have low scores on one of the problem-solving tests. Nonalcoholic participants showed a connection between higher post-stress cortisol levels and impaired memory, a finding supported by earlier research.

[340] Errico, A. L., King A. C., Lovallo W. R., & Parsons O. A. (2002).  Cortisol Dysregulation and Cognitive Impairment in Abstinent Male Alcoholics. Alcoholism: Clinical and Experimental Research. 26(8), 1198 - 1204.

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Prenatal dangers

Older news items (pre-2010) brought over from the old website

Too much licorice in pregnancy may affect child's IQ and behavior

A Finnish study involving 321 eight year old children has found that those whose mothers ate more than 500mg of glycyrrhizin per week (found in the equivalent of 100g of pure licorice) had significant decrements in verbal and visuospatial abilities and in narrative memory, compared to those whose mothers consumed less licorice. They were also more likely to have poor attention spans and show disruptive behaviour such as ADHD. The effects on cognitive performance appeared dose related (that is, higher consumption correlated with greater impairment). Glycyrrhizin may impair the placenta, allowing stress hormones to cross from the mother to the baby. These hormones (glucocorticoids) are thought to affect fetal brain development and have been linked to behavioural disorders in children. Consumption of licorice among young women is common in Finland.

Raikkonen, K., Pesonen, A., Heinonen, K., Lahti, J., Komsi, N., Eriksson, J. G., et al. (2009). Maternal Licorice Consumption and Detrimental Cognitive and Psychiatric Outcomes in Children. Am. J. Epidemiol., 170(9), 1137-1146. doi: 10.1093/aje/kwp272.

Vitamin C deficiency impairs early brain development

A guinea pig study has found that newborn guinea pigs subjected to moderate vitamin C deficiency had 30% fewer hippocampal neurons and markedly worse spatial memory than guinea pigs given a normal diet. For several reasons the neonatal brain is thought to be particularly vulnerable to even a slight lowering of the vitamin C level. Vitamin C deficiency is very common in some parts of the world, and even in wealthy nations occurs in an estimated 5-10% of the adult population.

Tveden-Nyborg, P. et al. 2009. Vitamin C deficiency in early postnatal life impairs spatial memory and reduces the number of hippocampal neurons in guinea pigs. American Journal of Clinical Nutrition, 90 (3), 540-546.

Children of older fathers perform less well in intelligence tests during infancy

Reanalysis of a dataset of over 33,000 children born between 1959 and 1965 and tested at 8 months, 4 years, and 7 years, has revealed that the older the father, the more likely the child was to have lower scores on the various tests used to measure the ability to think and reason, including concentration, learning, memory, speaking and reading skills. In contrast, the older the mother, the higher the scores of the child in the cognitive tests.

Saha, S. et al. 2009. Advanced paternal age is associated with impaired neurocognitive outcomes during infancy and childhood. PLoS Medicine 6(3), e1000040. doi:10.1371/journal.pmed.1000040 
Full text available at

Early maternal experience can affect memory in her offspring

A study of pre-adolescent mice with a genetically-created defect in memory has found that a mere two weeks exposure to a stimulating environment resulted in a reversal of the memory defect. But most surprisingly, it was also found that this effect was passed on to the next generation, even though they had the same genetic defect and even though they had no such experience themselves, and even when they were reared by other mice (not their mothers). It’s worth emphasising that the enrichment occurs for the mother long before she’s fertile, yet still benefits her offspring. The finding adds to many recent studies showing that genes are more malleable than we thought.

Arai, J., Li, S., Hartley, D.M. & Feig, L.A. 2009. Transgenerational Rescue of a Genetic Defect in Long-Term Potentiation and Memory Formation by Juvenile Enrichment. Journal of Neuroscience, 29(5), 1496-1502.

Breaking fish advice during pregnancy may benefit babies

Fears of the effects of mercury have led to government warnings to pregnant women to limit their consumption of seafood. However, a study involving nearly 12,000 women has found that children whose mothers ate the least amount of seafood during pregnancy showed the worst performance on tests of social development and verbal IQ, and beneficial effects were evident among children of women who ate more than the recommended guidelines.

Hibbeln, J.R. et al. 2007. Maternal seafood consumption in pregnancy and neurodevelopmental outcomes in childhood (ALSPAC study): an observational cohort study. The Lancet,369 (9561), 578-585.

Ingredient commonly found in shampoos may inhibit brain development

An ingredient found in many shampoos and other personal care products (Diethanolamine (DEA)) appears to interfere with normal brain development in baby mice when applied to the skin of their pregnant mothers. DEA appears to block the body's ability to absorb the nutrient choline, which is essential for normal development of the brain. Whether the amounts most people absorb from personal care products would cause harm remains unclear. A list of some products that contain DEA can be found at

Craciunescu, C.N., Wu, R. & Zeisel, S.H. 2006. Diethanolamine alters neurogenesis and induces apoptosis in fetal mouse hippocampus. FASEB Journal, 20, 1635-1640.

Lead exposure leads to brain cell loss and damage years later

A study of 532 former employees of a chemical manufacturing plant who had not been exposed to lead for an average of 18 years has found that the higher their lead levels were, the more likely they were to have smaller brain volumes and greater amounts of brain damage. 36% had white matter lesions. The results confirm earlier findings in this same population that people with occupational lead exposure experience declines in their thinking and memory skills years after their exposure.

Stewart, W.F. et al. 2006. Past adult lead exposure is linked to neurodegeneration measured by brain MRI. Neurology, 66, 1476-1484.

Prenatal exposure to urban air pollutants affects cognitive development

A study of 183 three-year-old children of non-smoking African-American and Dominican women residing in New York City has found that exposure during pregnancy to combustion-related urban air pollutants (specifically, polycyclic aromatic hydrocarbons) was linked to significantly lower scores on mental development tests and more than double the risk of developmental delay at age three.

Perera, F.P. et al. 2006. Effect of Prenatal Exposure to Airborne Polycyclic Aromatic Hydrocarbons on Neurodevelopment in the First Three Years of Life Among Inner-City Children. Environmental Health Perspectives, published online ahead of print.
Full text is available at

Prenatal exposure to marine toxin causes lasting damage

A rat study has found that a single dose of the naturally occurring marine toxin domoic acid caused subtle but permanent cognitive damage in rats exposed to the chemical before birth. The effect occurred at levels below those generally deemed safe, and suggest that the toxin might negatively affect unborn children at levels that do not cause symptoms in expectant mothers. It was already known that toxic doses of domoic acid can damage the hippocampus.

Levin, E.D., Pizarro, K., Pang, W.G., Harrison, J. & Ramsdell, J.S. 2005. Persisting behavioral consequences of prenatal domoic acid exposure in rats. Neurotoxicology and Teratology, in press.

Rats infected as newborns vulnerable to memory problems when infected in adulthood

Underscoring the value of good prenatal care, a new rat study has found that rats who experienced a one-time infection as newborns didn't learn as well as adult rats who were not infected as pups, after their immunity was challenged. The findings fit into a growing body of evidence that even a one-time infection can potentially permanently change physiological systems, a phenomenon called "perinatal programming." The findings implicate prenatal infections, as the rats were infected on their 4th day, a time that corresponds, in terms of brain development, with the 3rd trimester in humans. It should be noted that adult rats who were not infected as pups did not suffer memory impairment as the result of adult infection, and those who were infected as newborns were completely normal until they received the second immune system challenge in adulthood. It’s suggested that this phenomenon may help explain some of the individual variability in disease susceptibility.

Bilbo, S.D., Levkoff, L.H., Mahoney, J.H., Watkins, L.R., Rudy, J.W. & Maier, S.F. 2005. Neonatal Infection Induces Memory Impairments Following an Immune Challenge in Adulthood. Behavioral Neuroscience, 119 (1)

Prenatal exposure to solvents associated with negative cognitive effects

A study of 64 children aged 3 to 9 found that those children whose mothers were exposed to organic solvents during their pregnancies had lower scores on certain tests of language, behavior, and cognitive functioning. Organic solvents (used for example in dry cleaning, manufacturing, jobs involving paints and plastic adhesives, nail salons and medical laboratories) are some of the most common sources of workplace chemical exposure reported by pregnant women.

Laslo-Baker, D., Barrera, M., Knittel-Keren, D., Kozer, E., Wolpin, J., Khattak, S., Hackman, R., Rovet, J. & Koren, G. 2004. Child Neurodevelopmental Outcome and Maternal Occupational Exposure to Solvents. Archives of Pediatrics & Adolescent Medicine, 158, 956-961.

Environmental damage to brains of children

A new report suggests that the brains of children in many parts of Europe are suffering greater damage from environmental risks than previously recognized. A meeting in Malta of European delegates preparing for a ministerial conference on environment and health, being held in Budapest in June, were given preliminary results from a comprehensive study on environmental threats to children's health, being conducted by the WHO and the University of Udine, Italy. The full report is to be published at the Budapest conference. The findings suggest lead is the single most important damaging chemical for children. In 2001, the estimated percentage of European children in urban areas with elevated blood levels (above 10 micrograms per decilitre) ranged from 0.1% to 30.2%.

Vital role in brain development for the nutrient choline

The nutrient choline is known to play a critical role in memory and brain function by positively affecting the brain's physical development through increased production of stem cells (the parents of brain cells). New research demonstrates that this occurs through the effect of choline on the expression of particular genes. The important finding is that diet during pregnancy turns on or turns off division of stem cells that form the memory areas of the brain. Developing babies get choline from their mothers during pregnancy and from breast milk after they are born. Other foods rich in choline include eggs, meat, peanuts and dietary supplements. Breast milk contains much more of this nutrient than many infant formulas. Choline is a vitamin-like substance that is sometimes treated like B vitamins and folic acid in dietary recommendations.
A choline food database is available at:

Niculescu, M.D., Yamamuro, Y. & Zeisel, S.H. 2004. Choline availability modulates human neuroblastoma cell proliferation and alters the methylation of the promoter region of the cyclin-dependent kinase inhibitor 3 gene. Journal of Neurochemistry, 89 (5), 1252-1259.

Prenatal exposure to secondhand smoke associated with greater risk of developmental delay

A new study funded by the National Institute of Environmental Health Sciences has found that children whose mothers are exposed during pregnancy to second-hand smoke have reduced scores on tests of cognitive development at age two, when compared to children from smoke-free homes. In addition, the children exposed to second-hand smoke during pregnancy are approximately twice as likely to have developmental scores below 80, which is indicative of developmental delay. These differences were magnified for children whose mothers lived in inadequate housing or had insufficient food or clothing during pregnancy. The combined effect results in a developmental deficit of about seven points in tests of cognitive performance.

Rauh, V.A., Whyatt, R.M., Garfinkel, R., Andrews, H., Hoepner, L., Reyes, A., Diaz, D., Camann, D. & Perera, F.P. 2004. Developmental effects of exposure to environmental tobacco smoke and material hardship among inner-city children. Neurotoxicology and Teratology, 26 (3), 373-385.

Pre-term labor drug sensitizes brain to pesticide injury

A rat study has found that unborn rats exposed to terbutaline - a drug commonly prescribed to halt pre-term labor and stave off premature birth - suffered greater brain cell damage than those not given the drug upon secondary exposure to the common insecticide chlorpyrifos. This suggests that this drug might leave the brains of children susceptible to other chemicals ubiquitously present in the environment, and may help explain earlier suggestions that children whose mothers are administered terbutaline suffer cognitive deficits.

Rhodes, M.C., Seidler, F.J., Qiao, D., Tate, C.A., Cousins, M.M. & Slotkin, T.A. 2004. Does pharmacotherapy for preterm labor sensitize the developing brain to environmental neurotoxicants? Cellular and synaptic effects of sequential exposure to terbutaline and chlorpyrifos in neonatal rats. Toxicology and Applied Pharmacology, 195 (2), 203-217.

Impact of prenatal environment on learning abilities

In a fascinating study that points to the importance of environment (including prenatal environment) in determining behavioral and cognitive abilities, embryos from mice with a low response to stress were transferred to high-stress surrogate mice. The two strains of mice differed not only in their response to stress but also in their learning abilities. At birth, the mice were cross-fostered again and reared by either a low-stress mother or a high-stress mother. The mice were tested at three months, and researchers found that the low-stress mice that were transferred as embryos to and also later reared by high-stress females were less likely to explore new environments than those carried and reared by low-stress mothers. The low-stress mice reared by high-stress surrogates also performed more poorly on cognitive tests of their ability to navigate mazes.

Francis, D.D., Szegda, K., Campbell, G., Martin, W.D. & Insel, T.R. 2003. Epigenetic sources of behavioral differences in mice. Nature Neuroscience, 6 (5),445–446.

Fetuses recognize mother's voice in the womb

A study of 60 third-term fetuses found that they could distinguish between their mother’s voice and the voice of a stranger, as measured by changes in heart rate. Previous research has shown that newborns prefer their own mother's voice to that of a female stranger, but this demonstrates that this preference and recognition begins in the womb.

Kisilevsky, B.S., Hains, S.M.J., Lee, K., Xie, X., Huang, H., Ye, H.H., Zhang K. & Wang, Z. 2003. Effects of experience on fetal voice recognition. Psychological Science, 14 (3), 220-224(5).

Cognitive development affected in babies exposed prenatally to cocaine

In the first study to use measures of both the mothers’ self report of their prenatal drug use, and infant meconium, which provided a physical measure of the amount of drug exposure, 415 cocaine-exposed infants born in Cleveland were compared to non-exposed infants on cognitive and motor development until age 2. Infants were tested at 6.5, 12 and 24 months. Mental retardation in the cocaine-exposed children at age 2 was 4.89 times higher than would be expected in the general population. The percentage of children with mild delays requiring intervention was almost double the rate of the high risk, non-cocaine group. The study also found that tobacco exposure had significant negative effects on infant development.

Singe, L.T., Arendt, R., Minnes, S., Salvator, A., Kirchner, H.L., Farkas, K., & Kliegman, R. 2002. Cognitive and Motor Outcomes of Cocaine-Exposed Infants. Journal of the American Medical Association, 287,1952-1960.

Use of ecstasy during pregnancy may produce learning and memory impairments in child

Researchers today reported the first evidence that a mother’s use of MDMA (ecstasy) during pregnancy may result in specific types of long-term learning and memory impairments in her offspring.
The research was conducted by scientists from Children’s Hospital Research Foundation and the University of Cincinnati College of Medicine, on rats. It appears the damage to offspring occurs only if the drug is taken during a particular critical period of pregnancy.

Broening, H.W., Morford, L.L., Inman-Wood, S.L., Fukumura, M. & Vorhees, C.V. 2001. 3,4-Methylenedioxymethamphetamine (Ecstasy)-Induced Learning and Memory Impairments Depend on the Age of Exposure during Early Development. Journal of Neuroscience, 21, 3228-3235.

Prenatal exposure to Alcohol

Where math takes place normally and in children with fetal alcohol spectrum disorder

An imaging study involving 21 children with fetal alcohol spectrum disorder confirms the importance of the left parietal area for mathematical tasks. Children with FASD are particularly impaired in mathematical ability. Brain activity patterns also revealed that the involvement of regions in the left cerebellum and the brainstem in math processing may be specific to children with FASD.

[291] Lebel, C., Rasmussen C., Wyper K., Andrew G., & Beaulieu C.
(2010).  Brain Microstructure Is Related to Math Ability in Children With Fetal Alcohol Spectrum Disorder.
Alcoholism: Clinical and Experimental Research. 34(2), 354 - 363.

Possible genetic risk for fetal alcohol disorders

In partial explanation of why children who are exposed to alcohol because their mothers drank during pregnancy are differently affected, new research with rhesus monkeys has found evidence of a gene variant that appears to make the carrier more susceptible to the effects of fetal alcohol exposure. The gene involved is the serotonin transporter gene promoter, and this variant has previously been implicated in increased depression risk.

[499] Kraemer, G. W., Moore C. F., Newman T. K., Barr C. S., & Schneider M. L.
(2008).  Moderate Level Fetal Alcohol Exposure and Serotonin Transporter Gene Promoter Polymorphism Affect Neonatal Temperament and Limbic-Hypothalamic-Pituitary-Adrenal Axis Regulation in Monkeys.
Biological Psychiatry. 63(3), 317 - 324.

Post-natal choline supplements may reduce cognitive effects associated with prenatal alcohol exposure

A rat study has found that giving choline to rat pups exposed to alcohol during the equivalent of the third trimester, when there’s a spurt in brain growth, significantly reduced the severity of alcohol-related over-activity and spatial learning deficits. The benefits lasted months after choline treatment, suggesting that choline’s effects are long-lasting. Further studies are needed to establish exactly how choline helps and how late in development it can reduce fetal alcohol effects, and then, whether the effects also apply to humans. However, although early postnatal choline may reduce learning deficits and hyperactivity following early alcohol exposure, it doesn’t help reduce motor coordination deficits.

Thomas, J.D. et al. 2007. Choline Supplementation Following Third-Trimester Equivalent Alcohol Exposure Attenuates Behavioral Alterations in Rats. Behavioral Neuroscience, 121 (1), 120-130.

Eye movement tasks can be used to assess fetal alcohol spectrum disorders

Fetal alcohol spectrum disorders (FASD) cover a wide array of adverse developmental outcomes in children due to prenatal alcohol exposure and is harder to diagnose than the more severe Fetal Alcohol Syndrome. Now new research indicates than simple eye-movement tasks can be used to assess individuals with FASD.

Green, C.R. et al. 2007. Deficits in Eye Movement Control in Children With Fetal Alcohol Spectrum Disorders. Alcoholism: Clinical and Experimental Research, 31 (3), 500–511.

Numbers, sequences pose problems for Fetal Alcohol Syndrome children

An assessment of 50 Canadian children aged six to 15 years, who had been diagnosed with Fetal Alcohol Spectrum Disorder, has revealed that they had specific deficits in memory for numbers and sequences, which may contribute to common math difficulties faced by these children. The study also found differences between Aboriginal children and Caucasian children with FASD.

[1041] Rasmussen, C., Horne K., & Witol A.
(2006).  Neurobehavioral Functioning in Children with Fetal Alcohol Spectrum Disorder.
Child Neuropsychology. 12(6), 453 - 453.

Prenatal exposure to alcohol linked to lower I.Q.

Analysis of data from the Maternal Health Practices and Child Development Project, an examination of prenatal substance use among women who attended a prenatal clinic from 1983 to 1985, has found that even light to moderate drinking – especially during the second trimester – is associated with lower IQs in African-American offspring at 10 years of age, but not Caucasian children. The difference was not due to differences in the amount or pattern of alcohol use during pregnancy or by differences in socioeconomic status.

[364] Willford, J., Leech S., & Day N.
(2006).  Moderate prenatal alcohol exposure and cognitive status of children at age 10.
Alcoholism, Clinical and Experimental Research. 30(6), 1051 - 1059.

New 'eye movement' test may help treat fetal alcohol syndrome

At present there are no objective diagnostic tools that can be used to distinguish between children with Fetal Alcohol Spectrum Disorder (FASD) and those with other developmental disorders such as Attention-Deficit Hyperactivity Disorder (ADHD). Many of the behavioural tests used to assess children with FASD are geared to white, middle-class English-speaking people. Now a pilot study involving 25 children aged 8-12 has found that the specific brain abnormalities associated with FASD can be identified using a simple test that measures eye movement.

Reynolds, J. & Green, C. 2005. Presented at the annual meeting of the international Society for Neuroscience in Washington, D.C.

Key neural system at risk from fetal alcohol exposure

A study of pregnant rhesus monkeys has found that prenatal exposure to alcohol has pronounced effects on the development and function later in life of the brain's dopamine system. Dopamine is a key chemical messenger in the brain. The study indicates there is no safe dose, nor safe time to drink, for pregnant women. The monkeys consumed the equivalent of one to two drinks a day. Abnormalities in dopamine functioning can contribute to addiction, memory, attention and problem solving, and more pronounced conditions such as schizophrenia. The nature of the damage is significantly different depending on the timing of the alcohol exposure.

[511] Kraemer, G. W., Schneider M. L., Moore C. F., Barnhart T. E., Larson J. A., DeJesus O. T., et al.
(2005).  Moderate-Level Prenatal Alcohol Exposure Alters Striatal Dopamine System Function in Rhesus Monkeys.
Alcoholism: Clinical and Experimental Research. 29(9), 1685 - 1697.

Prenatal alcohol exposure can lead to lasting changes in cognitive processing

A study involving 337 African-American children, 7.5 years of age, selected from the Detroit Prenatal Alcohol Longitudinal Cohort, has found that although children known to have been prenatally exposed to moderate-to-heavy levels of alcohol were able to perform as well as other children when tasks were simple – such as naming colors within a timed period – when pressed to respond quickly while having to think about the response, their processing speed slowed down significantly. The observed deficits in working memory are thought to be partly a result of the slower processing speed. The study also confirmed earlier suggestions that number processing is particularly affected.

[946] Burden, M. J., Jacobson S. W., & Jacobson J. L.
(2005).  Relation of Prenatal Alcohol Exposure to Cognitive Processing Speed and Efficiency in Childhood.
Alcoholism: Clinical and Experimental Research. 29(8), 1473 - 1483.

Prenatal alcohol exposure has effects far beyond fetal alcohol syndrome

Numerous studies have documented IQ deficits in children with fetal alcohol syndrome (FAS). Little research, however, has found IQ deficits in children with alcohol-related neurodevelopmental disorder (ARND), who generally exhibit less severe neurobehavioral deficits than children with FAS. A new study demonstrates that what was interpreted in prior studies as a lack of any IQ effects in nonsyndromal, alcohol-exposed children was really due to a differential effect of exposure related to several risk/protective factors. Specifically, children whose mothers are older than 30 years, those whose mothers have alcohol dependence, those whose parents provide a less stimulating environment, and those whose mothers reported drinking during the time of conception, are at greater risk from prenatal alcohol exposure.

Jacobson, S.W., Jacobson, J.L., Sokol, R.J., Chiodo, L.M. & Corobana, R. 2004. Maternal Age, Alcohol Abuse History, and Quality of Parenting as Moderators of the Effects of Prenatal Alcohol Exposure on 7.5-Year Intellectual Function. Alcoholism: Clinical & Experimental Research, 28(11), 1732-1745.

New hope for children with fetal alcohol syndrome

A study of 415 people diagnosed with either fetal alcohol syndrome (FAS) or fetal alcohol effect (FAE) found two factors greatly increased the chances of escaping the negative experiences common to those with such problems - being diagnosed early in life and being raised in a stable and nurturing environment. These findings offer hope in a situation that many have regarded as hopeless.

[1051] Streissguth, A. P., Bookstein F. L., Barr H. M., Sampson P. D., O'Malley K., & Young J K.
(2004).  Risk factors for adverse life outcomes in fetal alcohol syndrome and fetal alcohol effects.
Journal of Developmental and Behavioral Pediatrics: JDBP. 25(4), 228 - 238.

Light drinking during pregnancy may lead to learning and memory deficits in adolescents

The dangers for the developing child of heavy drinking during pregnancy are well-known, but an ongoing longitudinal study of 580 children and their mothers has found that even light to moderate drinking may have significant effects on the cognitive development of the child – effects which show up in adolescents in subtle difficulties with learning and memory, specifically in the auditory/verbal domain.

Willford, J.A., Richardson, G.A., Leech, S.L. & Day, N.L. 2004. Verbal and Visuospatial Learning and Memory Function in Children With Moderate Prenatal Alcohol Exposure. Alcoholism: Clinical & Experimental Research, 28(3), 497-507.

Deficits associated with prenatal alcohol exposure can be seen as early as infancy

Most of the research on arousal and attention deficits caused by prenatal alcohol exposure has been conducted with children. A new study examined different components of attention through use of heart-rate data collected from six-month-old infants. The findings indicate that slower processing speeds and arousal-regulation problems exist as early as infancy.

Kable, J.A. & Coles, C.D. 2004. The Impact of Prenatal Alcohol Exposure on Neurophysiological Encoding of Environmental Events at Six Months. Alcoholism: Clinical & Experimental Research, 28(3), 489-496.

Prenatal exposure to alcohol affects executive functioning in young children

A study of 316 four-year-old children whose mothers had used various combinations of cocaine, alcohol, and/or marijuana during pregnancy, found that children in the alcohol-exposed group performed significantly worse at an inhibition task than the children in the control group (no maternal use of such substances during pregnancy). This effect persisted even after controlling for prenatal drug exposure, postnatal environmental factors, and child verbal IQ, and suggests that children exposed prenatally to alcohol find it more difficult to inhibit inappropriate behaviors. This may partly explain why such children are at greater risk for social and academic problems. The subtle effect may not be noticeable in most children, but for those who operate at lower levels of functioning, the effect may make all the difference between coping and not. This effect occurred with prenatal alcohol exposure of less than one drink per day. In the United States, it is estimated that among women who know they are pregnant, 2% continue to drink at a moderate level and 5% continue to have at least two drinks per week.

[560] Noland, J. S., Singer L. T., Arendt R. E., Minnes S., Short E. J., & Bearer C. F.
(2003).  Executive Functioning in Preschool-Age Children Prenatally Exposed to Alcohol, Cocaine, and Marijuana.
Alcoholism: Clinical and Experimental Research. 27(4), 647 - 656.

Motor skill training may help children with fetal alcohol exposure

The disorders associated with fetal exposure to alcohol are a leading cause of mental retardation and developmental delay.Research with rats has looked at the effect of motor skill training on the development of rats similarly exposed to alcohol at a critical stage of their prenatal development. Those rats trained in increasingly difficult challenges involving motor skills were found to develop 20% more synapses in the cerebellum than the rats that did not train, even though they had the expected 30% loss of Purkinje cells. The research brings hope that, despite the damage done to the motor function, it may be possible to rehabilitate these deficits if caught early enough.

[1369] Klintsova, A. Y., Scamra C., Hoffman M., Napper R. M. A., Goodlett C. R., & Greenough W. T.
(2002).  Therapeutic effects of complex motor training on motor performance deficits induced by neonatal binge-like alcohol exposure in rats: : II. A quantitative stereological study of synaptic plasticity in female rat cerebellum.
Brain Research. 937(1-2), 83 - 93.

tags development: 

tags lifestyle: 

tags problems: 

Cancer & the brain

Older news items (pre-2010) brought over from the old website

Helping 'chemobrain'

Mouse study points to possible treatment for chemobrain

A mouse study has found that four commonly used chemotherapy drugs disrupt neurogenesis, and that the condition could be partially reversed with the growth hormone IGF-1. Surprising the researchers, both the drugs which cross the blood-brain barrier (cyclophosphamide and fluorouracil) and the two that don’t (paclitaxel and doxorubicin) reduced neurogenesis, with fluorouracil producing a 15.4% reduction, compared to 22.4% with doxorubicin, 30.5% with cyclophosphamide, 36% with paclitaxel. A second study of a single high dose of cyclophosphamide, a mainstay of breast cancer treatment, resulted in a 40.9% reduction. Administration of the experimental growth hormone IGF-1 helped in all cases, but was more effective with the high dose.
[448] Gross, R. A., Janelsins M. C., Roscoe J. A., Berg M. J., Thompson B. D., Gallagher M. J., et al.
(2010).  IGF-1 partially restores chemotherapy-induced reductions in neural cell proliferation in adult C57BL/6 mice.
Cancer Investigation. 28(5), 544 - 553.

Stem cells restore cognitive abilities impaired by brain tumor treatment

A rat study has found that transplanted stem cells restored learning and memory to normal levels four months after radiotherapy. This compares with a greater than 50% decline in cognitive function in those rats that didn’t receive the therapy. Cranial irradiation is a common treatment for brain tumors.
[803] Acharya, M. M., Christie L. - A., Lan M. L., Donovan P. J., Cotman C. W., Fike J. R., et al.
(2009).  Rescue of radiation-induced cognitive impairment through cranial transplantation of human embryonic stem cells.
Proceedings of the National Academy of Sciences. 106(45), 19150 - 19155.

Exercise can aid recovery after brain radiation

A mouse study has found that exercise can prevent a decline in memory after whole-brain radiation treatment. Mice that had radiation plus access to a running wheel did as well at remembering where an escape hole in maze was as normal mice that didn't exercise. Irradiated mice that had no access to an exercise wheel eventually showed no particular preference for the section of the maze with the escape hole. The irradiated mice who didn’t exercise also showed depressive-like behavior, while those who exercised did not.
Wong-Goodrich, S.J. et al. 2009. Exercise promotes recovery from cognitive dysfunction, depressive-like behavior, and loss of hippocampal neurogenesis following whole-brain irradiation in adult mice. Presented October 20 at the annual Society for Neuroscience meeting in Chicago.

Potential remedy for the 'mental fog' in cancer patients

A rat study has found that injections of the antioxidant N-acetyl cysteine (a modified form of the dietary amino acid cysteine), fully prevented the memory loss induced by the commonly used chemotherapy drugs adriamycin and cyclophosphamide. The findings suggest that the cause of impairment is oxidative stress. More research will be needed to determine the safety of NAC for chemotherapy patients.
[846] Konat, G. W., Kraszpulski M., James I., Zhang H-T., & Abraham J.
(2008).  Cognitive dysfunction induced by chronic administration of common cancer chemotherapeutics in rats.
Metabolic Brain Disease. 23(3), 325 - 333.

Anastrozole does not impair cognition in postmenopausal women at risk of breast cancer

Trials have demonstrated that anastrozole is superior to tamoxifen in preventing breast cancer recurrence, and contralateral breast cancer in postmenopausal women, however other research has suggested that women receiving endocrine therapies show significantly poorer performance on verbal memory and processing tasks. In a substudy of the International Breast Intervention Study (IBIS II), which was specifically designed to investigate the clinical benefit of anastrozole, given daily for 5 years, as a primary chemopreventive treatment, cognitive function was assessed at baseline and at 6 and 24 months after the start of treatment. There were no significant differences between the anastrozole group and the placebo group in attention or memory, however, at 24 months significantly more women in the anastrozole group reported hot flushes. I note the recent study indicating the number of hot flushes in postmenopausal women is correlated with cognitive impairment.
[640] Jenkins, V. A., Ambroisine L. M., Atkins L., Cuzick J., Howell A., & Fallowfield L. J.
(2008).  Effects of anastrozole on cognitive performance in postmenopausal women: a randomised, double-blind chemoprevention trial (IBIS II).
The Lancet Oncology. 9(10), 953 - 961.

Narcolepsy drug alleviates post-chemotherapy fogginess

A trial involving 68 breast cancer survivors suffering from ‘chemo-brain’ has had positive results with modafinil (Provigil), a drug that promotes wakefulness. The women who took modafinil for eight weeks reported major improvements in memory, concentration and learning.
The findings were presented on June 3 at the American Society of Clinical Oncology meeting in Chicago.

Diabetes drug shows promise for preventing brain injury from radiation therapy

Hope for preventing the memory and learning problems that cancer patients often experience after whole-brain radiation treatments comes from a rat study. Rats receiving the diabetes drug piolitazone (Actos®) before, during and after radiation treatments did not experience cognitive impairment. The drug is thought to work by preventing inflammation.
[1156] Zhao, W., Payne V., Tommasi E., Diz D. I., Hsu F-C., & Robbins M. E.
(2007).  Administration of the peroxisomal proliferator-activated receptor gamma agonist pioglitazone during fractionated brain irradiation prevents radiation-induced cognitive impairment.
International Journal of Radiation Oncology, Biology, Physics. 67(1), 6 - 9.
Full text available at

Possible treatment found for 'chemobrain'

A common consequence of chemotherapy is memory problems, confusion and difficulty in concentrating ("chemobrain"). While nearly all breast and ovarian cancer patients receiving chemotherapy or radiation treatments seem to suffer chemobrain, 61% continue to experience memory problems long after their cancer treatment has stopped. A new study involving 154 cancer survivors suggests a possible new treatment using the drug dexmethyphenidate (d-MPH). The drug significantly reduced fatigue and improved memory.
Results of the study were presented to the annual meeting of the American Society of Clinical Oncology.

Estrogen boosts memory in men with prostate cancer

A new study suggests that high doses of estrogen may improve long-term memory and decrease feelings of confusion in men whose testosterone levels have been lowered to treat advanced prostate cancer. The findings suggest that hormone deprivation, prostate cancer or a combination of the two significantly impair verbal memory, while estrogen therapy significantly improves verbal memory performance. Hormone deprivation appears to slow working memory performance, but did not affect accuracy. Supplementation with estrogen did not affect working memory.
Beer, T.M. & Janowsky, J. 2004. High dose estrogen may enhance memory in men with prostate cancer. Presented at the American Society for Clinical Oncology annual meeting in New Orleans, La. on June 6.

Evidence for 'chemobrain'

Childhood brain tumors permanently impact cognition & lifestyle

A survey involving 785 CNS cancer survivors, 5,870 survivors of non-CNS cancers (such as leukemia, Hodgkin's disease, and bone tumors), and 379 siblings of CNS cancer survivors, sent at least 16 years after diagnosis, has found that CNS cancer survivors reported significantly greater neurocognitive dysfunction than their siblings and survivors of other types of cancer. Moreover, these problems were linked to lower achievement in education and in full-time employment and income, as well as less chance of being married. The worst problems were found in those who had tumors in the cortex, and those who had cranial radiation treatment.
Ellenberg, L. et al. 2009. Neurocognitive Status in Long-Term Survivors of Childhood CNS Malignancies: A Report From the Childhood Cancer Survivor Study. Neuropsychology, 23 (6), 705-717.
Full text available at

Whole-brain radiation therapy for tumors results in worse cognitive function

In a randomised controlled trial, 58 patients with one to three brain tumors were treated either with stereotactic radiosurgery (SRS) plus whole-brain radiotherapy (WBRT), or with SRS alone. Those who were randomly assigned to SRS plus WBRT were more likely to show a significant drop on a verbal learning & memory test at 4 months than patients randomly assigned to SRS alone (52% vs 24%, despite patients in the SRS alone group having a higher overall brain tumour recurrence rate. This finding persisted at 6-month follow-up. However, tumors didn’t recur in 73% of patients in the SRS plus WBRT group at 1 year, compared with 27% of patients who received SRS alone. Mortality rates were also higher in the SRS alone group. Despite this, the authors advise against WBRT because it causes more of decline in brain function — but point to the need for close clinical monitoring in that case (but see report below).
[1211] Maor, M. H., Chang E. L., Wefel J. S., Hess K. R., Allen P. K., Lang F. F., et al.
(2009).  Neurocognition in patients with brain metastases treated with radiosurgery or radiosurgery plus whole-brain irradiation: a randomised controlled trial.
The Lancet Oncology. 10(11), 1037 - 1044.
Full Article at:

Increased risk of cognitive problems for brain cancer patients who have whole brain radiation

A six-year study of 58 cancer patients with tumors that have spread to the brain has found that those who had whole brain radiation as well as stereotactic radiosurgery (SRS) had more than double the risk of developing learning and memory problems compared to those who only had stereotactic radiosurgery. The trial was halted when interim results showed that patients who received both had a 49% decline in learning and memory functioning at four months, while those who underwent stereotactic radiosurgery alone experienced only a 23% decline in neurocognitive functioning. Nearly half of the patients who had both treatments lost the ability to recall five words from the same list over three attempts.
The study was presented September 22, 2008, at the American Society for Therapeutic Radiology and Oncology's 50th Annual Meeting in Boston.

Chemotherapy may not affect memory in breast cancer patients

A study that tested 30 women with breast cancer repeatedly before each cycle of chemotherapy and one month after the final cycle, comparing them to healthy controls, found the women with breast cancer had slight problems in attention and learning skills before chemotherapy started. Only three women (10%) developed cognitive problems during chemotherapy, and interestingly, these were not the women who reported that they had problems.
Another study compared 40 women with breast cancer not yet treated, 27 women who had recently had a breast biopsy that was not cancerous, and 20 breast cancer survivors who had completed treatment at least one year before. On tests of working memory and spatial learning, the women recently diagnosed with breast cancer performed about the same as the women with the recent benign biopsy, but both groups were slower and less accurate than the breast cancer survivors. The results suggest the cognitive difficulties may be related to stress as a result of the diagnosis and other quality-of-life factors.
The studies were presented at the American Academy of Neurology Annual Meeting in Chicago, April 12–19.

Chemotherapy's damage to the brain identified

On the other hand, studies have shown that upwards of 82% of breast cancer patients report that they suffer from some form of cognitive impairment, and that a significant proportion of these (reports range from 15-20% to 50%) have lingering cognitive problems a year or more after treatment. And following their demonstration that three common chemotherapy drugs used to treat a wide range of cancers are more toxic to healthy brain cells than the cancer cells they were intended to treat, researchers have now found in cell and mouse studies that the widely used chemotherapy drug 5-fluorouracil (5-FU) is associated with a progressing collapse of support cells that are responsible for producing myelin. The next step will be to find out why some patients are vulnerable to this, and others not.
[935] Han, R., Yang Y. M., Dietrich J., Luebke A., Mayer-Pröschel M., & Noble M.
(2008).  Systemic 5-fluorouracil treatment causes a syndrome of delayed myelin destruction in the central nervous system.
Journal of Biology. 7(4), 12 - 12.
Full text available at

Cognitive deficits among cancer patients insufficiently recognized problem

A survey of 471 cancer patients has found that the cognitive impairment experienced by 14 to 45% of cancer patients can be long-lasting and severely affect their personal and professional lives. Patients report that the lack of concentration, short-term memory loss, difficulty with word recall and the inability to organize or multi-task have led to significant problems at home and in the workplace. 42% described their doctors as dismissive or indifferent when it came to addressing their concerns.
To view the executive summary, visit

How whole-brain radiation might cause dementia

Whole-brain radiation is widely used to treat recurrent brain tumors as well as to prevent other cancers from spreading to the brain. About a half of patients later develop progressive memory problems. A new study has now identified changes in brain chemistry that may be responsible. Using middle-aged rats, researchers found changes in brain receptors for the neurotransmitter glutamate. The changes may impair synaptic communication.
The research was reported at the annual meeting of the Radiation Research Society in Philadelphia.

Common cancer treatments toxic to healthy brain cells

A new study may explain ‘chemo-brain’ (cognitive dysfunction following chemotherapy). The study reveals that common drugs used to treat cancer are far more toxic to healthy brain cells than cancer cells — typical exposure levels killed 70-100% of brain cells but just 40-80% of the cancer cells. Moreover, the healthy cells continued to die for at least six weeks after treatment. Now the task is to find out how to protect healthy cells from the drugs.
The full article is available at:
[568] Dietrich, J., Han R., Yang Y., Mayer-Pröschel M., & Noble M.
(2006).  CNS progenitor cells and oligodendrocytes are targets of chemotherapeutic agents in vitro and in vivo.
Journal of Biology. 5(7), 22 - 22.

Chemotherapy temporarily affects the brain

A new study has found that although significant regions of the brain associated with cognitive function were significantly smaller in breast cancer patients within 12 months of receiving adjuvant chemotherapy, after three years, there were no differences in these regions between those who had received chemotherapy and those who had not.
[418] Uchitomi, Y., Inagaki M., Yoshikawa E., Matsuoka Y., Sugawara Y., Nakano T., et al.
(2007).  Smaller regional volumes of brain gray and white matter demonstrated in breast cancer survivors exposed to adjuvant chemotherapy.
Cancer. 109(1), 146 - 156.

Chemo drugs for treating breast cancer may cause changes in cognitive function

A study involving female mice confirms the existence of "chemobrain", finding mild to moderate learning and memory deficits in mice receiving methotrexate and 5-fluorouracil (5FU), two drugs widely used in women to prevent recurrence of breast cancer. The deficits extended only to those types of memory that involve the hippocampus or the frontal lobes (spatial memory and working memory, in this instance). The study only looked at short-term effects (2—4 weeks).
[1069] Winocur, G., Vardy J., Binns M. A., Kerr L., & Tannock I.
(2006).  The effects of the anti-cancer drugs, methotrexate and 5-fluorouracil, on cognitive function in mice.
Pharmacology Biochemistry and Behavior. 85(1), 66 - 75.

Brain scans reveal 'chemobrain' no figment of the imagination

A PET study of 21 women who had undergone surgery to remove breast tumors five to 10 years earlier found that the 16 who had been treated with chemotherapy regimens near the time of their surgeries to reduce the risk of cancer recurrence had specific alterations in activity of frontal cortex, cerebellum, and basal ganglia compared to 5 breast cancer patients who underwent surgery only, and 13 control subjects who did not have breast cancer or chemotherapy. The alterations suggested the chemotherapy patients’ brains were working harder to recall the same information.
[542] Ganz, P. A., Silverman D. H. S., Dy C. J., Castellon S. A., Lai J., Pio B. S., et al.
(2007).  Altered frontocortical, cerebellar, and basal ganglia activity in adjuvant-treated breast cancer survivors 5-10 years after chemotherapy.
Breast Cancer Research and Treatment. 103(3), 303 - 311.

Cancer survivors may be at higher risk for cognitive dysfunction

A study involving 702 cancer survivors and their cancer-free twins has found that cancer survivors are twice as likely to develop cognitive problems as individuals who have never been treated for cancer. About 15% of the cancer survivors showed cognitive dysfunction. The study did not involve patients who had tumors involving the central nervous system. A follow-up study is planned, to compare those who received different treatments for their cancer.
[284] Heflin, L. H., Meyerowitz B. E., Hall P., Lichtenstein P., Johansson B., Pedersen N. L., et al.
(2005).  Cancer as a risk factor for long-term cognitive deficits and dementia.
Journal of the National Cancer Institute. 97(11), 854 - 856. 

Impaired neuromotor function following cancer treatment can improve

A study of 142 patients who had blood disorders and who underwent hematopoietic cell transplant (preceded by high-dose chemotherapy) found that, at three months after transplant, patients experienced a significant decline in all cognitive and motor functions tested. By one year, however, the neuromotor functions for most patients had come back to the level experienced before the transplant, with the exception of two capabilities: grip strength and motor dexterity. Patients who had no chemotherapy or chemotherapy with only hydroxyurea prior to the transplant and those who did not receive certain immune suppressants were better off.
Syrjala, K.L., Dikmen, S., Langer, S.L., Roth-Roemer, S. & Abrams, J.R. 2004. Neuropsychologic changes from before transplantation to 1 year in patients receiving myeloablative allogeneic hematopoietic cell transplant. Blood, 104, 3386-3392.

New radiation therapy of brain tumors in children spares cognitive functions

The second phase of a clinical trial for ependymoma (a malignant brain tumor that occurs predominately in children) suggests a radiation therapy technique called conformal radiation therapy (CRT) allows young patients to enjoy normal development of their cognitive functions. About 75% of the 88 children treated for ependymoma with CRT did not experience progression of their cancer after three years, and their cognitive development was not significantly impaired by radiation therapy. Although radiation treatment is more effective than chemotherapy for brain tumors, physicians have been reluctant to use it because of fears of impairing cognitive development in young children.
[637] Boop, F. A., Sanford R. A., Merchant T. E., Mulhern R. K., Krasin M. J., Kun L. E., et al.
(2004).  Preliminary Results From a Phase II Trial of Conformal Radiation Therapy and Evaluation of Radiation-Related CNS Effects for Pediatric Patients With Localized Ependymoma.
J Clin Oncol. 22(15), 3156 - 3162.

Cognitive dysfunction found in women with breast cancer prior to treatment

The first study to evaluate cognitive skills prior to chemotherapy has found significant deficits in neuropsychological function in breast cancer patients before undergoing chemotherapy, and suggests the incidence of "chemobrain," a widely reported side effect in women undergoing treatment for breast cancer, may be overestimated. The study found 35% of the women demonstrated baseline cognitive impairment with significant deficits in verbal learning and memory prior to chemotherapy. Psychomotor processing speed and attention, non-verbal memory, naming, complex visual tasks and hand fine motor dexterity also trended toward significant impairment compared to the controls.
[544] Wefel, J. S., Lenzi R., Theriault R., Buzdar A. U., Cruickshank S., & Meyers C. A.
(2004).  'Chemobrain' in breast carcinoma?: a prologue.
Cancer. 101(3), 466 - 475.

tags problems: 

Post-surgery cognitive decline

Older news items (pre-2010) brought over from the old website

Cognitive decline after noncardiac surgery

Older surgical patients at greater risk for developing cognitive problems

There’s been quite a lot of research on the effects of cardiac surgery on cognitive function, but less is known about the effects of any surgery. Now a study of more than 1000 adult patients of different ages has tested memory and cognitive function before undergoing elective non-cardiac surgery, at the time of hospital discharge, and three months after surgery. It was found that many patients, regardless of age, experienced postoperative cognitive dysfunction (POCD) at the time they left the hospital (36.6% of young adults, 30.4% of the middle-aged, 41.4% of elderly). But three months later, those aged 60 and older were more than twice as likely to exhibit POCD (12.7% compared to less than 6% for both young and middle-aged). POCD was more common among those patients with lower educational level and a history of a stroke that had left no noticeable neurologic impairment. Those with POCD at both the time of hospital discharge and three months after surgery also were more likely to die within the first year after surgery. The reason for this is unclear, but it’s speculated that patients with prolonged cognitive dysfunction might be less able to take medicines correctly or may not recognize the need to seek medical care for symptoms of complications. [1]

Cognitive decline after heart bypass

More evidence bypass surgery not responsible for cognitive impairment

A 6-year study of 326 heart patients has found no differences in brain impairment between those who had on-pump coronary artery bypass surgery (152 patients), off-pump bypass surgery patients (75 patients), and those who had drugs and arterial stents to keep their blood vessels open instead of bypass surgery (99 patients). However, all of them were found to have experienced significant cognitive decline over the six-year study period on tests of verbal memory, visual memory, visuoconstruction, language, motor speed, psychomotor speed, attention, and executive function, when compared to 69 heart-healthy people who had no known risk factors for coronary artery disease. The findings provide more evidence that it is the disease and not the surgery that causes long-term cognitive problems. [2]

Long-term cognitive decline in bypass patients not due to surgery

Another study has come out supporting the view that coronary bypass patients have no greater risk of long-term cognitive decline than patients not undergoing surgery. The study involved 152 patients who had bypass surgery and 92 patients with coronary artery disease who did not have surgical intervention. Patients had memory and other cognitive tests at the beginning of the study period, and after 3, 12, 36 and 72 months. The results showed that there were no significant differences in cognitive scores between the two groups at the beginning of the study. Both groups showed modest decline in cognitive performance during the study period, but there were no significant differences in the degree of decline between the groups after six years. It was suggested that the decline in both groups was related to the presence of risk factors for vascular disease. [3]

Inflammatory system genes linked to cognitive decline after heart surgery

The finding that people with variants of two genes involved in the inflammatory system appear to be protected from suffering a decline in mental function following heart surgery raises the possibility that therapy involving drugs known to dampen the inflammatory response may be effective in preventing cognitive decline after heart surgery. The specific genes involved were those for C-reactive protein (which plays an important role in the body’s initial response to injury) and P-selectin (which helps recruit circulating white blood cells to the site of an injury). Patients with the variation of the C-reactive protein gene were 20.6% less likely to suffer mental decline, and patients with the P-selectin variant had a 15.2% risk reduction. The risk of cognitive decline for those with both gene variants was only 17% compared to 43% for patients who had neither variant. [4]

'Off-pump' CABG surgery appears to have no benefit on cognitive or cardiac outcomes at 5 years

A five-year study of 281 cardiac patients, half of whom received off-pump coronary artery bypass surgery and half on-pump surgery, has found that there was no difference in cognitive performance five years after surgery. The findings suggest that factors other than cardiopulmonary bypass may be responsible for cognitive decline, such as anesthesia and the generalized inflammatory response that is associated with major surgical procedures. [5]

Cognitive loss following coronary artery bypass surgery due to surgical technique?

A surgical strategy designed to minimize trauma to the body's largest artery – the aorta – during heart bypass surgery can significantly reduce cognitive loss that often follows the operation. The study found that at least 60% of patients showed neurological deficits following bypass surgery, but that at 6 months, 57% of patients who had traditional surgery still had deficits while only 32% of those who didn’t use the heart-lung machine during surgery, and 30% of those who had the new surgical technique still had deficits. Researchers conclude that surgical technique is the primary cause of cognitive decline following bypass surgery. [6]

Use of heart pump during bypass surgery not implicated in cognitive decline

A study involving 380 individuals has found that those patients undergoing coronary artery bypass grafting (CABG) surgery that used a cardiopulmonary heart pump had no significant differences in their mental functions compared to CABG patients whose surgery did not involve a heart pump. Patients with coronary heart disease all performed lower on cognitive tests than healthy controls, prior to surgery. By three months, both cardiac patients who had undergone surgery (with or without use of a heart pump) and those who had not, had improved cognitive function. [7]

Review finds bypass surgery free of long-term brain effects for most

A broad retrospective review of the effects of coronary artery bypass surgery on cognitive functions concludes that, although the research confirms the existence of mild deficits in the period up to three months after surgery, the procedure itself probably does not cause late or permanent neurological effects. Rather, they argue, the late cognitive declines seen in some long-term studies are for most people likely associated with progression of underlying conditions such as cerebrovascular disease. However, this is not true for all. The exceptions might include older patients and those with risk factors for cerebrovascular disease or a history of stroke. [8]

Elderly experience long-term cognitive decline after surgery

Researchers have found that two years after major non-cardiac surgery, 42% of elderly patients will have experienced a measurable cognitive decline. 59% of patients experienced cognitive decline immediately after surgery — these are the ones at greatest risk of long-term decline. Three months after surgery, 34% of patients had cognitive declines. The study involved 354 patients, with an average age of 69.5 years. [9]

Lower temperatures improve outcomes after bypass surgery

One of the possible adverse effects of cardiac bypass surgery is cognitive decline. Researchers have found that patients who were allowed an additional 10 to 12 minutes to return to normal body temperature after surgery scored almost one-third better on standard tests of cognition six weeks after surgery. (In order to protect the brain and other organs from damage while the heart is stopped during surgery, physicians cool a patient's blood as it passes through a heart-lung machine. However, toward the end of the operation, this blood needs to be rewarmed.) [10]

Cognitive decline after bypass surgery appears more transient than feared

Recent studies have found a high occurrence of cognitive problems in patients who undergo coronary artery bypass surgery, with such problems still found six weeks after surgery. In a new study comparing 140 patients who underwent bypass surgery and a second group of 92 coronary artery disease patients who did not have surgery, no differences in cognitive abilities were found when patients were re-tested at three and 12 months. This supports recent research suggesting that it is the disease itself that is the major problem, rather than the surgery. [11]

Lowered immunity puts older coronary bypass patients at higher risk for cognitive decline

Older patients with lowered immunity to certain common bacteria found in the gastrointestinal tract are more likely than younger patients to suffer cognitive decline after coronary artery bypass surgery. [12]

Cognitive impairment following bypass surgery may last longer than thought

More support for a link between cardiopulmonary bypass surgery and cognitive impairment comes from a new study. In particular, it seems, that attention may be most affected. The study also found evidence of longer-lasting cognitive decline than previously thought. Bypass patients also demonstrated poorer cognitive performance before the surgery, and it is now being suggested that it may be the disease itself that is the major problem, rather than the surgery itself. This is consistent with recent research connecting cardiovascular risk factors with risk factors for cognitive decline. [13]

Fever immediately after heart bypass surgery associated with cognitive decline

Elevated temperatures within 8-10 hours after surgery are often seen in patients who have undergone coronary bypass surgery. This has not however been regarded as anything other than a nuisance. Many bypass patients also suffer measurable cognitive decline. A new study reports on a relationship between these fevers and cognitive decline six weeks following surgery. Patients who suffered the highest post-operative temperatures also suffered the highest amount of cognitive decline. [14]

More on implications of having the Alzheimer's gene

Researchers have found an association between nerve cell changes associated with aging and the presence of a variation of the apolipoprotein gene known as apolipoprotein E4 (APOE4). This form is carried by approximately 25% of the population and has been linked to increased risk of Alzheimer's disease, cardiovascular disease and memory loss after head injury or bypass surgery. [15]

Frequency of cognitive decline after bypass surgery>

Heart bypasses are becoming increasingly common - in the U.S., more than half a million people undergo coronary-artery bypass grafting (CABG) each year. A common side-effect of the procedure is postoperative cognitive decline (frequency of occurrence estimates range from 33% to 82%, depending on the method of evaluation used). A recent study looked at the longer-term picture: in this study, cognitive decline was found in 53% of the patients at time of discharge; at 6 weeks, the rate was assessed at 36%; at 6 months, 24%. However, five years after the surgery the rate of cognitive decline was 42%. Older age, a lower level of education, a higher preoperative score for cognitive function, and the presence of cognitive decline at discharge were all predictors of cognitive decline at 5 years after CABG. Of these, the most significant predictor was a decline in cognition seen at discharge.
Note that there was no control group, so these results must be treated with caution. Note also that short-term declines in cognitive function are also reported in elderly subjects after non-cardiac surgery, and this can persist in a proportion of these patients - in fact, in 10% after 2 years. [16]

1.Monk, T.G. et al. 2008. Predictors of Cognitive Dysfunction after Major Noncardiac Surgery. Anesthesiology, 108(1), 18-30.
Price, C.C.; Garvan, C.W. & Monk, T.G. 2008. Type and Severity of Cognitive Decline in Older Adults after Noncardiac Surgery. Anesthesiology, 108(1), 8-17. Press release

2.Selnes, O.A. et al. 2009. Do Management Strategies for Coronary Artery Disease Influence 6-Year Cognitive Outcomes? Annals of Thoracic Surgery, 88, 445-454. Press release

3.Selnes, O.A. et al. 2008. Cognition 6 Years After Surgical or Medical Therapy for Coronary Artery Disease. Annals of Neurology, 63, 581-590. Press release Press release

4.Mathew, J.P. et al. 2007. Genetic Variants in P-Selectin and C-Reactive Protein Influence Susceptibility to Cognitive Decline After Cardiac Surgery. Journal of the American College of Cardiology, 49, 1934 - 1942. Press release

5.van Dijk, D. et al. 2007. Cognitive and Cardiac Outcomes 5 Years After Off-Pump vs On-Pump Coronary Artery Bypass Graft Surgery. JAMA, 297, 701-708. Press release

6.Hammon, J.W., Stump, D.A., Butterworth, J.F., Moody, D.M., Rorie, K., Deal, D.D., Kincaid, E.H., Oaks, T.E. & Kon, N.D. 2006. Single crossclamp improves 6-month cognitive outcome in high-risk coronary bypass patients: The effect of reduced aortic manipulation.The Journal of Thoracic and Cardiovascular Surgery, 131 (1), 114-121. Press release

7.McKhann, G.M., Grega, M.A., Borowicz, L.M.Jr, Bailey, M.M., Barry, S.J.E., Zeger, S.L., Baumgartner, W.A. & Selnes, O.A. 2005. Is there cognitive decline 1 year after CABG?: Comparison with surgical and nonsurgical controls. Neurology, 65, 991-999. Press release

8.Selnes, O.A. & McKhann, G.M. 2005. Neurocognitive Complications after Coronary Artery Bypass Surgery. Annals of Neurology, Published Online: April 25, 2005 (DOI: 10.1002/ana.20481) Press release

9.Monk, T. et al. 2004. Paper presented October 26 at the annual scientific sessions of the American Society of Anesthesiologists in Las Vegas. Press release

10.Grocott, H. et al. 2004. Paper presented April 26 at the annual scientific sessions of the Society of Cardiovascular Anesthesiologists. Press release

11.Selnes, O.A., Grega, M.A., Borowicz, L.M. Jr , Royall, R.M., McKhann, G.M. & Baumgartner, W.A. 2003. Cognitive changes with coronary artery disease: a prospective study of coronary artery bypass graft patients and nonsurgical controls. The Annals of Thoracic Surgery, 75 (5), 1377-1386. Press release

12.Mathew, J.P., Grocott, H.P., Phillips-Bute, B., Stafford-Smith, M., Laskowitz, D.T., Rossignol, D., Blumenthal, J.A. & Newman, M.F. 2003. Lower Endotoxin Immunity Predicts Increased Cognitive Dysfunction in Elderly Patients After Cardiac Surgery. Stroke, 34, 508. Press release

13.Keith, J.R., Puente, A.E., Malcolmson, K.L., Tartt, S., Coleman, A.E. & Marks, H.F. Jr. 2002. Assessing Postoperative Cognitive Change After Cardiopulmonary Bypass Surgery. Neuropsychology, 16(3), 411-21. Press release

14.Grocott, H.P., Mackensen, G.B., Grogore, A.M., Mathew, J., Reves, J.G., Phillips-Bute, B., Smith, P.K. & Newman, M.F. 2002. Postoperative Hyperthermia Is Associated With Cognitive Dysfunction After Coronary Artery Bypass Graft Surgery. Stroke, 33, 537-541. Press release

15.Doraiswamy, P.M. et al. 2002. Paper presented February 25 at the 15th annual meeting of the American Association for Geriatric Psychiatry in Orlando, Fla. Press release

16.Newman, M. F., Kirchner, J. L., Phillips-Bute, B., Gaver, V., Grocott, H., Jones, R. H., Mark, D. B., et al. (2001). Longitudinal Assessment of Neurocognitive Function after Coronary-Artery Bypass Surgery. N Engl J Med, 344(6), 395-402. Press release

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Several large, long-running studies have found that smoking significantly increases your risk of Alzheimer's, as does high exposure to secondhand smoke. Smoking, both in old age and in adolescence, is also associated with lower IQs and lower cognitive performance. It appears, however, that this is largely recoverable if you give up smoking.

Smoking has a particularly negative effect in conjunction with alcohol (and unfortunately they are often found in tandem). While moderate drinking can in some circumstances have positive effects on the brain, this is probably not the case for those who smoke. Moreover, smoking makes it much harder for the brain to recover from the effects of alcohol abuse and the damage done to the brain by heavy alcohol consumption is likely to be much worse if the individual is a smoker.

Older news items (pre-2010) brought over from the old website

Second-hand smoke linked to cognitive impairment

Smoking is known to be a risk factor for cognitive impairment and dementia. Now a large study of some 4800 non-smoking adults over the age of 50 has revealed that exposure to second-hand smoke (measured by levels of a nicotine by-product in their saliva) is associated with an increased chance of developing cognitive impairment, including dementia.

[641] Llewellyn, D. J., Lang I. A., Langa K. M., Naughton F., & Matthews F. E.
(2009).  Exposure to secondhand smoke and cognitive impairment in non-smokers: national cross sectional study with cotinine measurement.
BMJ. 338(feb12_2), b462 - b462.

The open-access article is available here.

Midlife smokers may have worse memory than non-smokers

Data from the very large Whitehall II study has found that those who smoked were more likely to be in the lowest 20% for cognitive performance compared with those who had never smoked. Those who reported being ex-smokers at the beginning of the study were 30% less likely than smokers to have poor vocabulary and low verbal frequency scores, showing that recovery is likely if smoking is stopped. The study also found a higher risk of death as well as non-participation in cognitive tests among smokers, suggesting the association between smoking and cognition may have been under-estimated.

[476] Sabia, S., Marmot M., Dufouil C., & Singh-Manoux A.
(2008).  Smoking History and Cognitive Function in Middle Age From the Whitehall II Study.
Arch Intern Med. 168(11), 1165 - 1173.

Smokers are more likely to develop dementia

A seven-year study of some 7,000 people age 55 and older found that those who were current smokers at the time of the study were 50% more likely to develop dementia than people who had never smoked or past smokers. Smoking did not increase the risk for those with the Alzheimer’s gene apolipoprotein E4. Current smokers without the gene were nearly 70% more likely to develop Alzheimer’s than nonsmokers or past smokers without the gene.

[2381] Reitz, C., den Heijer T., van Duijn C., Hofman A., & Breteler M. M. B.
(2007).  Relation between smoking and risk of dementia and Alzheimer disease.
Neurology. 69(10), 998 - 1005.

Secondhand smoke increases risk of dementia

Preliminary findings from the Cardiovascular Health Study indicates that elderly people with high lifetime exposure to secondhand smoke (more than 30 years) were approximately 30% more likely to develop dementia than those with no lifetime secondhand smoke exposure. People with abnormalities of their carotid arteries and high lifetime exposure to secondhand smoke were nearly two-and-a-half times as likely to develop dementia as those with no secondhand smoke exposure and no indications of carotid artery disease.

Haight presented the findings at the American Academy of Neurology’s 59th Annual Meeting in Boston, April 28 – May 5, 2007.

Smoking now found detrimental for Alzheimer’s

Previous animal studies had suggested that nicotine reduces the number of amyloid plaques; a new study, however, has found that chronic nicotine exposure increases neurofibrillary tangles.

[2380] Oddo, S., Caccamo A., Green K. N., Liang K., Tran L., Chen Y., et al.
(2005).  Chronic nicotine administration exacerbates tau pathology in a transgenic model of Alzheimer's disease.
Proceedings of the National Academy of Sciences of the United States of America. 102(8), 3046 - 3051.

Smoking associated with working memory impairment in adolescents

A study of 41 adolescent daily smokers and 32 nonsmokers has revealed that adolescent smokers had impairments in accuracy of working memory performance. Male adolescents as a group begin smoking at an earlier age than female smokers and were significantly more impaired during tests of selective and divided attention. All of the adolescent smokers also showed further disruption of working memory when they stopped smoking.

[1252] Jacobsen, L. K., Krystal J. H., Mencl E. W., Westerveld M., Frost S. J., & Pugh K. R.
(2005).  Effects of smoking and smoking abstinence on cognition in adolescent tobacco smokers.
Biological Psychiatry. 57(1), 56 - 66.

Smoking is bad for the brain

465 participants in the Scottish Mental Survey (11 year olds tested in 1947), approximately half of whom were smokers, were tested again when they were 64. Smokers performed significantly worse in five different cognitive tests than did both former smokers and those who had never smoked. This drop in cognitive function held when factors such as education, occupation and alcohol consumption were taken into account. A link between impaired lung function and cognitive ageing has long been suspected, though the mechanism is unclear.

[2382] Whalley, L. J., Fox H. C., Deary I. J., & Starr J. M.
(2005).  Childhood IQ, smoking, and cognitive change from age 11 to 64 years.
Addictive Behaviors. 30(1), 77 - 88.

Smoking and alcohol

Smoking may counteract benefit of moderate drinking on stroke risk

A 12-year study following the drinking and smoking habits of 22,524 people aged 39-79 has found that in non-smokers, people who consumed moderate amounts of alcohol were 37% less likely to develop stroke than non-drinkers. This association was not found among smokers. The finding may explain the inconsistency in previous studies into the relationship between light to moderate drinking and stroke.

The findings were presented at the American Academy of Neurology's 62nd Annual Meeting in Toronto, April 10 - 17, 2010.

Smoking interferes with recovery from alcohol-related brain damage

Another study has come out with more evidence that smoking makes it a lot harder for the brain to recover from the effects of long-term heavy drinking. The study looked specifically at changes in blood flow in the brain — blood flow is affected by alcohol use disorders. The study found that after 5 weeks of abstinence, alcohol-dependent individuals who didn’t smoke showed significantly improved blood flow, but those who smoked showed essentially no change. Moreover, the number of cigarettes smoked daily was correlated with how poorly the blood was flowing in the frontal lobe.

[1045] Mon, A., Durazzo T. C., Gazdzinski S., & Meyerhoff D. J.
(2009).  The impact of chronic cigarette smoking on recovery from cortical gray matter perfusion deficits in alcohol dependence: longitudinal arterial spin labeling MRI.
Alcoholism, Clinical and Experimental Research. 33(8), 1314 - 1321.

Alzheimer's starts earlier for heavy drinkers, smokers

A study of nearly 1000 people diagnosed with possible or probable Alzheimer’s disease has found that those who were heavy drinkers developed Alzheimer’s 4.8 years earlier than those who were not, while heavy smokers developed the disease 2.3 years sooner than people who were not heavy smokers. Those with the APOE å4 gene developed the disease three years sooner than those without the gene variant. The risk factors are additive — those with all three risk factors developed the disease 8.5 years earlier than those with none of the risk factors.

The research was presented at the American Academy of Neurology Annual Meeting in Chicago, April 12 – April 19.

Nicotine may enhance attention and working memory in recovering alcoholics

New findings show that nicotine patches may enhance cognitive functioning among newly recovering alcoholics with a history of smoking. Nicotine (but not tobacco) has been shown to have a cognitive benefit, particularly on attention processes. The study also found that alcoholics who smoked were more sensitive to the drug dose of nicotine than were community controls who also smoked.

[1006] Nixon, S J., Lawton-Craddock A., Tivis R., & Ceballos N.
(2007).  Nicotine's Effects on Attentional Efficiency in Alcoholics.
Alcoholism: Clinical and Experimental Research. 31(12), 2083 - 2091.

Smoking interferes with brain's recovery from alcoholism

In another study indicating smoking worsens the effect of alcoholism on the brain, smoking was found to apparently interfere with the brain's ability to recover from the effects of chronic alcohol abuse.

[2371] Durazzo, T. C., Gazdzinski S., Rothlind J. C., Banys P., & Meyerhoff D. J.
(2006).  Brain Metabolite Concentrations and Neurocognition During Short‐term Recovery from Alcohol Dependence: Preliminary Evidence of the Effects of Concurrent Chronic Cigarette Smoking.
Alcoholism: Clinical and Experimental Research. 30(3), 539 - 551.

Long-term smoking associated with dulled thinking and lower IQ

A long-term study involving 172 alcoholic and non-alcoholic men has found that long-term smoking impaired memory and reasoning skills and reduced IQ. The effect was most pronounced among those who had smoked for years. The effects of smoking were found among the non-alcoholics as well as the alcoholics, and among the alcoholics, the cognitive impact of long-term heavy smoking appeared to be greater than the impact of drinking.

[1116] Glass, J. M., Adams K. M., Nigg J. T., Wong M. M., Puttler L. I., Buu A., et al.
(2006).  Smoking is associated with neurocognitive deficits in alcoholism.
Drug and Alcohol Dependence. 82(2), 119 - 126.

Smoking seems to increase brain damage in alcoholics

Another study has come out indicating that alcoholics who smoke are at greater risk of brain damage. The imaging study compared brain volume in recovered alcoholics and light drinkers. The study found no difference between smokers and non-smokers among the light drinkers, but among the alcoholics, the more severe the tobacco habit, the more brain volume had been lost.

[1049] Gazdzinski, S., Durazzo T. C., Studholme C., Song E., Banys P., & Meyerhoff D. J.
(2005).  Quantitative Brain MRI in Alcohol Dependence: Preliminary Evidence for Effects of Concurrent Chronic Cigarette Smoking on Regional Brain Volumes.
Alcoholism: Clinical and Experimental Research. 29(8), 1484 - 1495.

Cigarette smoking exacerbates alcohol-induced brain damage

Heavy alcohol consumption is known to cause brain damage. A new imaging study has compared 24, one-week-abstinent alcoholics (14 smokers, 10 nonsmokers) in treatment with 26 light-drinking "controls" (7 smokers, 19 nonsmokers), and found that cigarette smoking can both exacerbate alcohol-induced damage as well as independently cause brain damage. The damage is most prominent in the frontal lobes (important in planning, decision-making, and multi-tasking among other functions). Independent of alcohol consumption, cigarette smoking also had adverse effects on brain regions involved in fine and gross motor functions and balance and coordination. Roughly 80% of alcohol-dependent individuals report smoking regularly.

[2370] Durazzo, T. C., Gazdzinski S., Banys P., & Meyerhoff D. J.
(2004).  Cigarette Smoking Exacerbates Chronic Alcohol‐Induced Brain Damage: A Preliminary Metabolite Imaging Study.
Alcoholism: Clinical and Experimental Research. 28(12), 1849 - 1860.

Benefits of nicotine

Nicotine patch may alleviate 'senior moments'

A small preliminary clinical trial has found that four weeks of nicotine skin patches helped decision-making and attention in people with age-associated memory impairment (the mildest form of cognitive impairment in seniors). Given the health risks of smoking, and health risks associated with nicotine patches, it is too early to recommend the use of nicotine to improve memory, however. Nicotine mimics the brain chemical acetylcholine, a nerve signal that plays a role in learning and memory.

[2383] White, H. K., & Levin E. D.
(2004).  Chronic transdermal nicotine patch treatment effects on cognitive performance in age-associated memory impairment.
Psychopharmacology. 171(4), 465 - 471.

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Sleep deprivation eliminates fear generalization

January, 2011

In a small study, a sleepless night after trauma prevents the development of PTSD symptoms.

Given all the research showing the importance of sleep for consolidating memories, it should come as no great surprise that the reverse is also true: depriving yourself of sleep could help you forget experiences you would prefer not to remember.

In the study, 28 student volunteers were shown 14 short video clips, half of which showed safe driving down a city street, and half showed the car being involved in a nasty crash. Half of the volunteers were then deprived of sleep while the other half received a normal night's sleep. The next day, they were shown pictures and asked to indicate whether they had appeared in the clips they had seen. They were also asked to rate the fear evoked by the image, and their physiological responses measured. They were tested again 3 and 10 days later.

While there was no difference between the two groups in picture recognition, the control group rated the images from the crash videos as fearful, and these responses generalized over time to the other images. However, those who were sleep deprived showed such reactions only on the first day.

The finding suggests a possible therapy for PTSD or other anxiety disorders.





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