Sleep deprivation

Latest Research News

Chronic insomnia linked to memory problems

Data from 28,485 older Canadians (45+) found that those with chronic insomnia performed significantly worse on cognitive tests than those who had symptoms of insomnia without any noticable impact on their daytime functioning and those with normal sleep quality. The main type of memory affected was declarative memory (memory of concepts, events and facts).

Chronic insomnia is characterized by trouble falling asleep or staying asleep at least three nights a week for over three months with an impact on daytime functioning (mood, attention, and daytime concentration).

https://www.eurekalert.org/pub_releases/2019-05/cu-cia051519.php

Poor brainwave syncing behind older adults failure to consolidate memories

We know that memories are consolidated during sleep, and that for some reason this consolidation becomes more difficult with age. Now a new study shows why.

To consolidate memories (move them into long-term storage), low and speedy brain waves have to sync up at exactly the right moment during sleep. These brain rhythms synchronize perfectly in young adults, but in old age, it seems, slow waves during non-rapid eye movement (NREM) sleep are not so good at making timely contact with the speedy electrical bursts known as “spindles.”

These difficulties are thought to be due to atrophy of the gray matter in the medial frontal cortex.

The study compared the overnight memory of 20 healthy young adults to that of 32 healthy older adults (mostly in their 70s). Before going to sleep, participants learned and were then tested on 120 word sets. They were tested again in the morning. EEG results from their sleeping brains showed that in older people, the spindles consistently peaked early in the memory-consolidation cycle and missed syncing up with the slow waves.

http://www.futurity.org/memories-sleep-older-adults-1633432/

https://www.eurekalert.org/pub_releases/2017-12/uoc--obd121417.php

Oxidative stress governs sleep

A fruitfly study has shown how oxidative stress leads to sleep. Fruitflies (and, it is believed, humans) have sleep-control neurons that act like an on-off switch: if the neurons are electrically active, the fly is asleep; when they are silent, the fly is awake. The switch is triggered, it appears, by an electrical current that flows through two ion channels, and this, it now appears, is regulated by a small molecule called NADPH.

The state of NADPH reflects the degree of oxidative stress. Sleeplessness causes oxidative stress, driving the behavior of NADPH.

I'm wildly speculating here, but is it possible that increased sleep problems often found with age are linked to a growing inability of this molecule to sensitively monitor the degree of oxidative stress, perhaps due to high levels of oxidative stress??

https://www.eurekalert.org/pub_releases/2019-03/uoo-saa032119.php

Disrupted sleep in one's 50s, 60s raises Alzheimer's risk

A study involving 95 healthy older adults found that adults reporting a decline in sleep quality in their 40s and 50s had more amyloid-beta in their brains later in life, while those reporting poorer sleep in their 50s and 60s had more tau tangles. Those with high levels of tau protein were more likely to lack the synchronized brain waves during deep NREM sleep that are associated with a good night's sleep, and the more tau protein, the less synchronized these brain waves were.

Previous research has found that a dip in the amplitude of slow wave activity during deep NREM sleep was associated with higher amounts of beta-amyloid in the brain and memory impairment.

https://www.eurekalert.org/pub_releases/2019-06/uoc--dsi062619.php

Studies of healthy animals and humans have reported higher levels of amyloid beta after a single night of sleep deprivation, and that disruption of slow-wave sleep causes amyloid beta levels to rise as much as 30%. Moreover, a single night’s sleep deprivation has been found to increase tau levels by as much as 50% in cerebrospinal fluid.

These findings suggest that quality sleep helps the body clear excess amyloid and tau proteins.

https://www.eurekalert.org/pub_releases/2019-03/aps-spa032119.php

A preliminary study involving 20 healthy subjects aged 22 to 72 found beta-amyloid increases of about 5% after losing a night of sleep.

Many researchers believe the link between sleep disorders and Alzheimer's risk is "bidirectional," since elevated beta-amyloid may also lead to sleep disturbances.

https://www.eurekalert.org/pub_releases/2018-04/nioa-los041318.php

A very small study involving eight people aged 30-60, who experienced (over time) two or three different sleep situations, found that amyloid beta levels were 25-30% higher when individuals had a a sleepless night — putting those amyloid beta levels on par with the levels seen in people genetically predisposed to develop Alzheimer’s at a young age.

http://www.futurity.org/sleep-alzheimers-amyloid-beta-1642332/

A sleep study involving 17 healthy adults aged 35 to 65, found that those whose slow-wave sleep was disrupted (by a beeping sound that moved them into a shallower sleep) found a 10% increase in amyloid beta levels after a single night of interrupted sleep, but no corresponding increase in tau levels. However, participants whose activity monitors showed they had slept poorly at home for the week before showed a spike in levels of tau.

http://www.futurity.org/sleep-alzheimers-proteins-1485152-2/

https://www.theguardian.com/science/2017/jul/10/poor-sleep-increases-risk-of-alzheimers-research-reveals

Is too much sleep an early sign of dementia?

Data from 2,457 older adults (65+) in the Framingham study found that those who consistently slept more than nine hours every night had twice the risk of developing dementia and Alzheimer’s disease within the next 10 years, compared to those who slept less than nine hours a night.

Over the 10-year study period, 234 were diagnosed with dementia.

It’s suggested that one reason might be that those with depression tend to sleep longer. In any case, it’s thought that the longer sleep sessions reflect something else going on, rather than being a cause.

Education level also affected the degree of risk. Those without a high school degree who slept more than nine hours nightly had a 600% greater risk of later receiving a dementia diagnosis than people with a high school degree.

http://www.futurity.org/too-much-sleep-dementia-1439122/

Optimal sleep linked to lower dementia risk

A ten-year Japanese study involving 1,517 older adults (60+) found that dementia rates were higher in those with daily sleep duration of less than 5 hours or more than 10 hours, compared with those with daily sleep duration of 5-6.9 hours. However, those with short sleep duration who had high physical activity did not have a greater risk of dementia.

294 participants (19%) developed dementia in the 10 year period.

https://www.eurekalert.org/pub_releases/2018-06/w-osl060518.php

Lack of REM sleep linked to higher dementia risk

A study involving 321 older adults (60+; average age 67), who participated in a sleep study between 1995 and 1998, found poorer REM sleep was associated with an increased risk of developing dementia over 12 years.

During that period, 32 people were diagnosed with some form of dementia (24 with Alzheimer’s)

Those who developed dementia spent an average of 17% of their sleep time in REM sleep, compared with 20% for those who didn’t develop dementia. For every percent that REM sleep was reduced, there was a 9% increase in dementia risk, and an 8% increase in Alzheimer’s risk specifically.

No such associations were found for other stages of sleep, although that shouldn’t be taken to mean that other sleep stages don’t affect key features of Alzheimer’s.

http://www.futurity.org/rem-sleep-dementia-risk-1524842/

Sleep apnea linked to higher tau levels

A study involving 288 cognitively healthy older adults (65+) found that those who had sleep apneas had on average 4.5% higher levels of tau in the entorhinal cortex than those who did not have apneas, after controlling for several other factors that could affect levels of tau in the brain, such as age, sex, education, cardiovascular risk factors and other sleep complaints.

15% (43 participants) were reported by their bed partners as having sleep apneas.

This preliminary study was presented at the American Academy of Neurology's 71st Annual Meeting in Philadelphia, May 4-10, 2019.

https://www.eurekalert.org/pub_releases/2019-03/aaon-sam022619.php

Data from 1,752 older adults found that sleep-disordered breathing was associated with poorer attention and processing speed. In particular, increased overnight hypoxemia (oxygen saturation below 90%) was linked with poorer attention and memory, and more daytime sleepiness associated with poorer attention and memory and slower cognitive processing speed.

These associations were strongest in APOE-ε4 carriers.

https://www.eurekalert.org/pub_releases/2017-07/ats-sdm071817.php

[4468] Winer, J. R., Mander B. A., Helfrich R. F., Maass A., Harrison T. M., Baker S. L., et al.
(2019).  Sleep as a Potential Biomarker of Tau and β-Amyloid Burden in the Human Brain.
Journal of Neuroscience. 39(32), 6315 - 6324.

[4469] Ning, S., & Jorfi M.
(2019).  Beyond the sleep-amyloid interactions in Alzheimer’s disease pathogenesis.
Journal of Neurophysiology. 122(1), 1 - 4.

[4413] Shokri-Kojori, E., Wang G-J., Wiers C. E., Demiral S. B., Guo M., Kim S. Won, et al.
(2018).  β-Amyloid accumulation in the human brain after one night of sleep deprivation.
Proceedings of the National Academy of Sciences. 115(17), 4483 - 4488.

[4470] Lucey, B. P., Hicks T. J., McLeland J. S., Toedebusch C. D., Boyd J., Elbert D. L., et al.
(2018).  Effect of sleep on overnight cerebrospinal fluid amyloid β kinetics.
Annals of Neurology. 83(1), 197 - 204.

[4471] Ju, Y-E. S., Ooms S. J., Sutphen C., Macauley S. L., Zangrilli M. A., Jerome G., et al.
(2017).  Slow wave sleep disruption increases cerebrospinal fluid amyloid-β levels.
Brain. 140(8), 2104 - 2111.

[4438] Westwood, A. J., Beiser A., Jain N., Himali J. J., DeCarli C., Auerbach S. H., et al.
(2017).  Prolonged sleep duration as a marker of early neurodegeneration predicting incident dementia.
Neurology. 88(12), 1172.

[4473] Ohara, T., Honda T., Hata J., Yoshida D., Mukai N., Hirakawa Y., et al.
(2018).  Association Between Daily Sleep Duration and Risk of Dementia and Mortality in a Japanese Community.
Journal of the American Geriatrics Society. 66(10), 1911 - 1918.

[4474] Pase, M. P., Himali J. J., Grima N. A., Beiser A. S., Satizabal C. L., Aparicio H. J., et al.
(2017).  Sleep architecture and the risk of incident dementia in the community.
Neurology. 89(12), 1244.

[4472] Johnson, D. A., Lane J., Wang R., Reid M., Djonlagic I., Fitzpatrick A. L., et al.
(2017).  Greater Cognitive Deficits with Sleep-disordered Breathing among Individuals with Genetic Susceptibility to Alzheimer Disease. The Multi-Ethnic Study of Atherosclerosis.
Annals of the American Thoracic Society. 14(11), 1697 - 1705.

 

Obstructive sleep apnea (OSA) occurs when a person's breathing is interrupted during sleep.

People with OSA are known to suffer memory problems and also have higher rates of depression.

A new study connects the two by finding that people with untreated OSA had problems recalling specific details about their lives. Previous research has established that persistent depression is associated with overly general autobiographical memories, where people don't remember many specific details of life events.

It may be that sleep apnea impairs the ability to either encode or consolidate certain types of life memories.

The study, involvidng 44 adults with untreated OSA and 44 healthy age-matched controls (average age 49), found that those with OSA had significantly more overgeneral memories: 52.3% compared with 18.9% of the controls.

OSA participants also had significantly poorer semantic recall of early adult life (facts from your personal history, like the names of your school teachers).

Across both groups, being older was associated with having a higher number of overgeneral autobiographical memories while higher depression was linked to having worse semantic memory.

https://www.eurekalert.org/pub_releases/2019-01/ru-sac013119.php

Poor sleep has been associated with Alzheimer's disease risk, but a new study suggests a specific aspect of sleep is important.

The study, involving 119 older adults (60+), of whom 80% were cognitively normal and the remainder very mildly impaired, found that decreased slow-wave sleep coincided with higher levels of tau in the brain and a higher tau-to-amyloid ratio in the cerebrospinal fluid.

Amyloid plaques and tau tangles develop for decades before cognitive symptoms of dementia emerge. Identifying the process at an early stage offers a possible window of opportunity for successful intervention.

Participants’ sleep at home was monitored over the course of a normal week, and participants also kept sleep logs of nighttime sleep and daytime napping. Thirty-eight people underwent PET brain scans for amyloid-beta and tau proteins, and 104 people underwent spinal taps to provide cerebrospinal fluid. Twenty-seven did both.

Those with increased tau pathology actually slept more, during both night and day, but their quality of sleep was poorer. In fact, daytime napping alone was significantly associated with high levels of tau, making it a useful indicator of risk.

https://www.futurity.org/alzheimers-disease-sleep-1954732/

Untreated sleep apnea in children shrinks brain & may slow development

Brain scans of children who have moderate or severe obstructive sleep apnea have found significant reductions of gray matter across the brain.

The study compared brain scans from 16 children (aged 7-11) with obstructive sleep apnea to those from nine healthy children of the same age, gender, ethnicity and weight, who did not have apnea. The scans were also compared to 191 MRI scans of children who were part of an existing database.

The brains of those children with OSA showed reduced gray matter in multiple brain regions, including the frontal, prefrontal, and parietal cortices, temporal lobe, and the brainstem.

Sleep apnea is known to affect cognition in adults, but it may be that it is even more damaging in brains that are still developing. However, adult studies have also shown that treating sleep apnea reverses gray matter loss and improves cognition. This finding therefore emphasizes the importance of treating children's sleep apnea.

Sleep apnea affects up to 5% of all children (and we can only assume that this will get more common, if childhood obesity continues to rise).

Developing brain regions in children are hardest hit by sleep deprivation

Another study of sleep deprivation in children gives weight to the idea that it is particularly important for proper brain development that children get good sleep.

The study measured the brain activity in 13 healthy five to 12-year-olds as they slept. On the first occasion, the children went to bed at their normal bedtime; the second time, they stayed awake until late and thus received exactly half the normal amount of sleep.

The results indicate that children's brains respond to sleep deprivation differently than adults’ brains do. In adults, being deprived of sleep creates a greater need for deep sleep, which is manifested in greater slow-wave activation in the prefrontal cortex. In the children's brains, this slow-wave increase occurred in the back regions of the brain, in the parietal and occipital lobes. This suggests that these areas might be especially vulnerable to sleep deprivation.

Moreover, this difference was linked to levels of myelin in part of the visual system. Myelin increases as the brain matures. Those with higher levels of myelin in certain nerve fibers in the visual system displayed slow-wave activation that was more similar to that of adults.

The researchers conclude that adequate sleep is important for neuronal connections to develop properly.

Poor sleep in early childhood may lead to cognitive, behavioral problems in later years

A study involving 1,046 children whose sleep was assessed at various points in their first seven years has found that children who didn’t get enough sleep in their preschool and early school years were more likely to have problems with attention, emotional control and peer relationships at age seven.

Sleep was assessed through interviews with the mothers when their children were around 6 months, 3 years and 7 years old, and from questionnaires completed when the children were ages 1, 2, 4, 5 and 6. Mothers and teachers filled out questionnaires evaluating each child's executive function and behavioral issues at around 7.

Children living in homes with lower household incomes and whose mothers had lower education levels were more likely to sleep less than nine hours at ages 5 to 7. Other factors associated with insufficient sleep include more television viewing, a higher body mass index, and being African American.

Insufficient sleep was defined as being less than the recommended amount of sleep at specific age categories:

  • 12 hours or longer at ages 6 months to 2 years
  • 11 hours or longer at ages 3 to 4 years
  • 10 hours or longer at 5 to 7 years.

https://www.eurekalert.org/pub_releases/2017-03/uocm-usa031517.php

https://www.eurekalert.org/pub_releases/2016-10/uoz-dbr100416.php

https://www.eurekalert.org/pub_releases/2016-11/f-hkb112816.php

https://www.eurekalert.org/pub_releases/2017-03/mgh-psi030917.php

A mouse study has found that mice (genetically engineered for Alzheimer’s) who were sleep deprived for eight weeks, not only showed significant cognitive impairment, but also showed a significant increase in the amount of tau protein that became phosphorylated and formed tangles. The other main characteristic of Alzheimer’s, amyloid-beta plaques, was not affected.

The findings are consistent with growing evidence of a link between sleep disturbance and Alzheimer’s, and suggests that chronic sleep disturbance accelerates Alzheimer’s pathology, and should be treated.

The sleep-deprived mice were given 20 hours of light each day, while the control mice were kept on a schedule of 12 hours of light and 12 hours of darkness.

http://www.eurekalert.org/pub_releases/2014-03/tu-csd031714.php

A study involving mice lacking a master clock gene called Bmal1 has found that as the mice aged, their brains showed patterns of damage similar to those seen in Alzheimer's disease and other neurodegenerative disorders. Many of the injuries seemed to be caused by free radicals. Several key antioxidant enzymes, which usually neutralize and help clear free radicals from the brain, have been found to peak in the middle of the day in healthy mice, but not in these mice lacking Bmal1. It may be that, without this daily increase, free radicals remain in the brain longer, causing more damage.

The finding may help explain the connection between sleep problems and Alzheimer’s.

http://www.eurekalert.org/pub_releases/2013-11/wuso-bc112513.php

[3594] Musiek, E. S., Lim M. M., Yang G., Bauer A. Q., Qi L., Lee Y., et al.
(2013).  Circadian clock proteins regulate neuronal redox homeostasis and neurodegeneration.
Journal of Clinical Investigation. 123(12), 5389 - 5400.

An Italian study has found that a significant percentage of Alzheimer’s patients suffer from Obstructive Sleep Apnea Syndrome. This respiratory disorder, which causes people to temporarily stop breathing during their sleep, affects cerebral blood flow, promoting cognitive decline. The finding adds to evidence that detecting and treating OSA early is important for preventing cognitive decline and dementia.

http://www.eurekalert.org/pub_releases/2013-10/ip-apn100813.php

Buratti, L. et al. 2013. Vascular Impairment in Alzheimer’s Disease: The Role of Obstructive Sleep Apnea. Journal of Alzheimer's Disease, 38 (2), 445-53.

Data from 70 older adults (average age 76) in the Baltimore Longitudinal Study of Aging has found that those who reported poorer sleep (shorter sleep duration and lower sleep quality) showed a greater buildup of amyloid-beta plaques.

http://www.eurekalert.org/pub_releases/2013-10/tjnj-lsa101813.php

[3606] Spira, A. P., Gamaldo A. A., An Y., & et al
(2013).  Self-reported sleep and β-amyloid deposition in community-dwelling older adults.
JAMA Neurology. 70(12), 1537 - 1543.

A study involving genetically engineered fruit flies adds to our understanding of why sleep and bioclock disruptions are common in those with Alzheimer's disease. People with Alzheimer's often have poor biological rhythms — periods of sleep become shorter and more fragmented, resulting in periods of wakefulness at night and snoozing during the day. It has been thought that Alzheimer’s destroys the biological clock, but this new study indicates that the clock is still working — however, it’s being ignored by other parts of the brain.

http://www.eurekalert.org/pub_releases/2014-02/uoc-swu022514.php

[3560] Chen, K-F., Possidente B., Lomas D. A., & Crowther D. C.
(2014).  The central molecular clock is robust in the face of behavioural arrhythmia in a Drosophila model of Alzheimer’s disease.
Disease Models & Mechanisms. 7(4), 445 - 458.

A small study involving 18 individuals with at least one mild traumatic brain injury with related sleep disturbance has shown that six weeks of morning bright light therapy resulted in a marked decrease in subjective daytime sleepiness, and improved nighttime sleep.

Sleep, because of its role in brain plasticity, is likely to be important for brain recovery, but unfortunately sleep problems are common in those with TBI.

The research was presented on June 3, in Baltimore, Md., at SLEEP 2013, the 27th annual meeting of the Associated Professional Sleep Societies LLC.

http://www.eurekalert.org/pub_releases/2013-05/aaos-blt053013.php

A new study adds to growing evidence of a link between sleep problems and Alzheimer’s. The interesting thing is that this association – between sleep apnea and Alzheimer’s biomarkers — wasn’t revealed until the data was separated out according to BMI.

Those with sleep apnea and a BMI under 25 showed several Alzheimer’s biomarkers (increased levels of tau in the cerebrospinal fluid, greater atrophy of the hippocampus, glucose hypometabolism in regions vulnerable to Alzheimer’s). This (with the exception of glucose hypometabolism in the mediotemporal lobe only) was not found in those with sleep apnea and a higher BMI.

The study involved 68 healthy older adults (average age 71), of whom 18 had normal breathing, 33 mild sleep apnea, and 17 moderate-severe apnea. Those in the latter group tended to have higher BMIs.

Some 10-20% of middle-aged adults in the U.S. have sleep apnea, and this jumps dramatically in those over 65 (30-60%), where the link to obesity is much smaller. The researchers suggest that early preclinical Alzheimer’s damage might be a reason, and plan follow-up research to assess what impact CPAP therapy for sleep apnea has on the Alzheimer’s biomarkers.

Those interested in the relationship between poor sleep and later development of Alzheimer’s might also like to read a Guardian article on the subject.

http://www.eurekalert.org/pub_releases/2013-05/ats-sft051413.php

Osorio, R.S. et al. 2013. Sleep-Disordered Breathing, Aging And Risk For Alzheimer's Disease In Cognitively Normal Subjects. Abstract 38456. Presented at the ATS 2013 International Conference.

The issue of ‘chemo-brain’ — cognitive impairment following chemotherapy — has been a controversial one. While it is now (I hope) accepted by most that it is, indeed, a real issue, there is still an ongoing debate over whether the main cause is really the chemotherapy. A new study adds to the debate.

The study involved 28 women who received adjuvant chemotherapy for breast cancer, 37 who received radiotherapy, and 32 age-matched healthy controls. Brain scans while doing a verbal working memory task were taken before treatment and one month after treatment.

Women who underwent chemotherapy performed less accurately on the working memory task both before treatment and one month after treatment. They also reported a significantly higher level of fatigue. Greater fatigue correlated with poorer test performance and more cognitive problems, across both patient groups and at both times (although the correlation was stronger after treatment).

Both patient groups showed reduced function in the left inferior frontal gyrus, before therapy, but those awaiting chemotherapy showed greater impairment than those in the radiotherapy group. Pre-treatment difficulty in recruiting this brain region in high demand situations was associated with greater fatigue after treatment.

In other words, reduced working memory function before treatment began predicted how tired people felt after treatment, and how much their cognitive performance suffered. All of which suggests it is not the treatment itself that is the main problem.

But the fact that reduced working memory function precedes the fatigue indicates it’s not the fatigue that’s the main problem either. The researchers suggest that the main driver is level of worry —worry interfered with the task; level of worry was related to fatigue. And worry, as we know, can reduce working memory capacity (because it uses up part of it).

All of which is to say that support for cancer patients aimed at combating stress and anxiety might do more for ‘chemo-brain’ than anything else. In this context, I note also that there have been suggestions that sleep problems have also been linked to chemo-brain — a not unrelated issue!

Cimprich, B. et al. 2012. Neurocognitive impact in adjuvant chemotherapy for breast cancer linked to fatigue: A Prospective functional MRI study. Presented at the 2012 CTRC-AACR San Antonio Breast Cancer Symposium, Dec. 4-8

Cancer survivors who underwent chemotherapy often suffer long-term cognitive problems. Until now, most research has been occupied with establishing that this is in fact the case, and studies investigating how to help have been rare. I recently reported on studies suggesting that help with sleep problems and stress can be beneficial. It has also been suggested that exercise can help. None of these suggestions are special to cancer survivors (although cancer survivors may well be one of several groups that derive particular benefit). Similarly, a new study investigates another familiar approach to improving cognitive decline.

The pilot study involved 82 post-menopausal breast cancer survivors (average age 56) who had received chemotherapy and who were worried about their cognitive abilities. The women were randomly assigned to one of three groups: one group received memory training adapted from the ACTIVE (Advanced Cognitive Training for Independent and Vital Elderly) trial; another received processing speed training using Posit Science’s Insight program (commercially available); the third was a wait-listed control group.

Training consisted of ten 1-hour small-group (3-5 people) sessions over 6-8 weeks. Memory training involved learning strategies and applying them to word lists, sequences, and texts. Strategies included mnemonic techniques, as well as instruction in principles of meaningfulness, organization, visualization, and association. Strategies were taught and practiced in the first five sessions, and further practiced in the remaining sessions.

In the Insight program, stimulus duration is progressively shortened during a series of progressively more difficult information-processing tasks, such as time-order judgment, discrimination, spatial-match, forward-span, instruction-following, and narrative-memory tasks. Exercises automatically adjust to maintain an 85% correct rate.

Both programs proved beneficial. The memory training group showed significant improvement in immediate and delayed memory, which was maintained at the two-month follow-up. There was of course individual variability: 39% showed significant improvement on immediate memory (compared to 18% of controls) and 42% on delayed memory (compared to 11% of controls). While the group as a whole didn’t show significant improvement in processing speed, some 73% of the group showed reliable improvement at the two-month follow-up.

The Insight group showed significant improvement on both memory and processing speed. Some 68% improved processing speed (compared to 43% of controls). But note that at the 2-month follow-up, the 67% of the Insight group is not that much greater than the 61% of the controls (demonstrating very clearly the benefits of even the small amount of practice received in testing) and is in fact less than the 73% of the memory group.

The Insight group also showed significant improvement in memory. At two-month follow-up, some 30% of the Insight group had improved immediate memory (compared to the 18% of controls), and 33% had improved delayed memory (vs 11%).

Both training programs had a positive effect on perceived cognitive functioning and symptom distress (mood, anxiety, fatigue), and there was no difference between the groups in terms of satisfaction with the training (both groups were very satisfied).

The researchers concluded that, while both training programs were promising, the dual effect of processing speed training (on memory as well as processing speed) argued for its broader benefits.

However, I note that, although the size of the effect of memory training on processing speed was too small to reach statistical significance, the fact that the number of participants showing reliable improvement was greater than that of the Insight group points to an equally broad effect of memory training. If the memory training was supplemented by a small amount of practice on tasks designed to boost processing speed, it would seem to me that this might produce greater cognitive benefits than the processing speed training. Indeed, the Insight program was, I believe, first developed in the context of the ACTIVE program, and I have, of course, talked before about the value of training that includes multiple domains.

Still, the main message of this study should not be overlooked: it demonstrates that many cancer survivors suffering from cognitive decline can improve their cognitive performance through training and practice.

I reported a few months ago on some evidence of a link between disturbed sleep and the development of Alzheimer’s. Now a mouse study adds to this evidence.

The mouse study follows on from an earlier study showing that brain levels of amyloid beta naturally rise when healthy young mice are awake and drop after they go to sleep, and that sleep deprivation disrupted this cycle and accelerated the development of amyloid plaques. This natural rhythm was confirmed in humans.

In the new study, it was found that this circadian rhythm showed the first signs of disruption as soon as Alzheimer’s plaques began forming in the mice’s brains. When the genetically engineered mice were given a vaccine against amyloid beta, the mice didn’t develop plaques in old age, the natural fluctuations in amyloid beta levels continued, and sleep patterns remained normal.

Research with humans in now underway to see whether patients with early markers of Alzheimer’s show sleep problems, and what the nature of these problems is.

Just to make it clear: the point is not so much that Alzheimer’s patients are more likely to have sleep problems, but that the sleep problems may in fact be part of the cause of Alzheimer’s disease development. The big question, of course, is whether you can prevent its development by attacking the dysfunction in circadian rhythm. (See more on this debate at Biomed)

Now that we’ve pretty much established that sleep is crucial for consolidating memory, the next question is how much sleep we need.

A new study compared motor sequence learning in 16 people with mild obstructive sleep apnea to a matched control group (also attending the sleep clinic). There were no significant differences between the groups in total sleep time, sleep efficiency and sleep architecture (time spent in the various sleep stages), subjective measures of sleepiness, or performance on a psychomotor vigilance task (a task highly sensitive to sleep deprivation).

Nor were there any differences in learning performance during the training phase on the motor task.

But the interesting thing about consolidation is that skills usually improve overnight — your performance the next day will usually be better than it was at the end of your training. And here there was a significant difference between the groups, with the controls showing much greater overnight improvement on the motor sequence task. For sequences learned in the morning and tested 12 hours later on the same day, however, there were no differences between the groups.

So given all the factors relating to sleep that were the same between the two groups, what was the factor behind the group consolidation difference? It turns out it was (principally) the arousal index (arousals were scored on the basis of abrupt shifts in EEG frequency that last at least 3 seconds with 10 seconds of stable sleep preceding), and to a lesser extent the apnea-hypopnea index.

It seems likely, then, that arousals from sleep may (depending, presumably, on timing) interrupt the transfer of labile memories from the hippocampus to the neocortex for long-term storage. Thus, the more arousals you have, the more likely it is that this process will be interrupted.

Older adults who sleep poorly react to stress with increased inflammation

A study involving 83 older adults (average age 61) has found that poor sleepers reacted to a stressful situation with a significantly greater inflammatory response than good sleepers. High levels of inflammation increase the risk of several disorders, including cardiovascular disease and diabetes, and have been implicated in Alzheimer’s.

Each participant completed a self-report of sleep quality, perceived stress, loneliness and medication use. Around 27% were categorized as poor sleepers. Participants were given a series of tests of verbal and working memory designed to increase stress, with blood being taken before and after testing, as well as three more times over the next hour. The blood was tested for levels of a protein marker for inflammation (interleukin-6).

Poor sleepers reported more depressive symptoms, more loneliness and more perceived stress compared to good sleepers. Before cognitive testing, levels of IL-6 were the same for poor and good sleepers. However, while both groups showed increases in IL-6 after testing, poor sleepers showed a significantly larger increase — as much as four times larger and at a level found to increase risk for illness and death in older adults.

After accounting for loneliness, depression or perceived stress, this association remained. Surprisingly, there was no evidence that poor sleep led to worse cognitive performance, thus causing more stress. Poor sleepers did just as well on the tests as the good sleepers (although I note that we cannot rule out that poor sleepers were having to put in more effort to achieve the same results). Although there was a tendency for poor sleepers to be in a worse mood after testing (perhaps because they had to put in more effort? My own speculation), this mood change didn’t predict the increased inflammatory response.

The findings add to evidence that poor sleep (unfortunately common as people age) is an independent risk factor for cognitive and physical health, and suggest we should put more effort into dealing with it, rather than just accepting it as a corollary of age.

REM sleep disorder doubles risk of MCI, Parkinson's

A recent Mayo Clinic study has also found that people with rapid eye movement sleep behavior disorder (RBD) have twice the risk of developing mild cognitive impairment or Parkinson’s disease. Some 34% of those diagnosed with probable RBD developed MCI or Parkinson's disease within four years of entering the study, a rate 2.2 times greater than those with normal REM sleep.

Earlier research has found that 45% of those with RBD developed MCI or Parkinson's disease within five years of diagnosis, but these findings were based on clinical patients. The present study involved cognitively healthy older adults (70-89) participating in a population-based study of aging, who were diagnosed for probable RBD on the basis of the Mayo Sleep Questionnaire.

A study involving 75 perimenopausal women aged 40 to 60 has found that those with memory complaints tended to show impairments in working memory and attention. Complaints were not, however, associated with verbal learning or memory.

Complaints were also associated with depression, anxiety, somatic complaints, and sleep disturbance. But they weren’t linked to hormone levels (although estrogen is an important hormone for learning and memory).

What this suggests to me is that a primary cause of these cognitive impairments may be poor sleep, and anxiety/depression. A few years ago, I reported on a study that found that, although women’s reports of how many hot flashes they had didn’t correlate with memory impairment, an objective measure of the number of flashes they experienced during sleep did. Sleep, as I know from personal experience, is of sufficient importance that my rule-of-thumb is: don’t bother looking for any other causes of attention and memory deficits until you have sorted out your sleep!

Having said that, depressive symptoms showed greater relationship to memory complaints than sleep disturbance.

It’s no big surprise to hear that it is working memory in particular that is affected, because what many women at this time of life complain of is ‘brain fog’ — the feeling that your brain is full of cotton-wool. This doesn’t mean that you can’t learn new information, or remember old information. But it does mean that these tasks will be impeded to the extent that you need to hold on to too many bits of information. So mental arithmetic might be more difficult, or understanding complex sentences, or coping with unexpected disruptions to your routine, or concentrating on a task for a long time.

These sorts of problems are typical of those produced by on-going sleep deprivation, stress, and depression.

One caveat to the findings is that the study participants tended to be of above-average intelligence and education. This would protect them to a certain extent from cognitive decline — those with less cognitive reserve might display wider impairment. Other studies have found verbal memory, and processing speed, impaired during menopause.

Note, too, that a long-running, large population study has found no evidence for a decline in working memory, or processing speed, in women as they pass through perimenopause and menopause.

A small study of the sleep patterns of 100 people aged 45-80 has found a link between sleep disruption and level of amyloid plaques (characteristic of Alzheimer’s disease). The participants were recruited from the Adult Children Study, of whom half have a family history of Alzheimer’s disease.

Sleep was monitored for two weeks. Those who woke frequently (more than five times an hour!) and those who spent less than 85% of their time in bed actually asleep, were more likely to have amyloid plaques. A quarter of the participants had evidence of amyloid plaques.

The study doesn’t tell us whether disrupted sleep leads to the production of amyloid plaques, or whether brain changes in early Alzheimer's disease lead to changes in sleep, but evidence from other studies do, I think, give some weight to the first idea. At the least, this adds yet another reason for making an effort to improve your sleep!

The abstract for this not-yet-given conference presentation, or the press release, don’t mention any differences between those with a family history of Alzheimer’s and those without, suggesting there was none — but since the researchers made no mention either way, I wouldn’t take that for granted. Hopefully we’ll one day see a journal paper providing more information.

The main findings are supported by another recent study. A Polish study involving 150 older adults found that those diagnosed with Alzheimer’s after a seven-year observation period were more likely to have experienced sleep disturbances more often and with greater intensity, compared to those who did not develop Alzheimer’s.

Ju, Y., Duntley, S., Fagan, A., Morris, J. & Holtzman, D. 2012. Sleep Disruption and Risk of Preclinical Alzheimer Disease. To be presented April 23 at the American Academy of Neurology's 64th Annual Meeting in New Orleans.

Bidzan L, Grabowski J, Dutczak B, Bidzan M. 2011. [Sleep disorders in the preclinical period of the Alzheimer's disease]. Psychiatria Polska, 45(6), 851-60. http://www.ncbi.nlm.nih.gov/pubmed/22335128

One survey of nearly 200 undergraduate college students who were not living with a parent or legal guardian found that 55% reported getting less than seven hours sleep. This is consistent with other surveys. The latest study confirms such a result, but also finds that students tend to think their sleep quality is better than it is (70% of students surveyed described their sleep as "fairly good" or better). It’s suggested that this disconnect arises from students making comparisons in an environment where poor sleep is common — even though they realized, on being questioned, that poor sleep undermined their memory, concentration, class attendance, mood, and enthusiasm.

None of this is surprising, of course. But this study did something else — it tried to help.

The researchers launched a campuswide media campaign consisting of posters, student newspaper advertisements and a "Go to Bed SnoozeLetter", all delivering information about the health effects of sleep and tips to sleep better, such as keeping regular bedtime and waking hours, exercising regularly, avoiding caffeine and nicotine in the evening, and so on. The campaign cost less than $2,500, and nearly 10% (90/971) said it helped them sleep better.

Based on interviews conducted as part of the research, the researchers compiled lists of the top five items that helped and hindered student sleep:

Helpers

  • Taking time to de-stress and unwind
  • Creating a room atmosphere conducive to sleep
  • Being prepared for the next day
  • Eating something
  • Exercising

Hindrances

  • Dorm noise
  • Roommate (both for positive/social reasons and negative reasons)
  • Schoolwork
  • Having a room atmosphere not conducive to sleep
  • Personal health issues

In another study, this one involving 142 Spanish schoolchildren aged 6-7, children who slept less than 9 hours and went to bed late or at irregular times showed poorer academic performance. Regular sleep habits affected some specific skills independent of sleep duration.

69% of the children returned home after 9pm at least three evenings a week or went to bed after 11pm at least four nights a week.

And a recent study into the effects of sleep deprivation points to open-ended problem solving being particularly affected. In the study, 35 West Point cadets were given two types of categorization task. The first involved cate­gorizing drawings of fictional animals as either “A” or “not A”; the second required the students to sort two types of fic­tional animals, “A” and “B.” The two tests were separated by 24 hours, during which half the students had their usual night’s sleep, and half did not.

Although the second test required the students to learn criteria for two animals instead of one, sleep deprivation impaired performance on the first test, not the second.

These findings suggest the fault lies in attention lapses. Open-ended tasks, as in the first test, require more focused attention than those that offer two clear choices, as the second test did.

News reports on sleep deprivation are collated here.

[2521] Orzech, K. M., Salafsky D. B., & Hamilton L A.
(2011).  The State of Sleep Among College Students at a Large Public University.
Journal of American College Health. 59, 612 - 619.

[2515] Cladellas, R., Chamarro A., del Badia M M., Oberst U., & Carbonell X.
(2011).  Efectos de las horas y los habitos de sueno en el rendimiento academico de ninos de 6 y 7 anos: un estudio preliminarEffects of sleeping hours and sleeping habits on the academic performance of six- and seven-year-old children: A preliminary study.
Cultura y Educación. 23(1), 119 - 128.

Maddox WT; Glass BD; Zeithamova D; Savarie ZR; Bowen C; Matthews MD; Schnyer DM. The effects of sleep deprivation on dissociable prototype learning systems. SLEEP 2011;34(3):253-260.

Sleep can boost classroom performance of college students

There’s a lot of evidence that memories are consolidated during sleep, but most of it has involved skill learning. A new study extends the findings to complex declarative information — specifically, information from a lecture on microeconomics.

The study involved 102 university undergraduates who had never taken an economics course. In the morning or evening they completed an introductory, virtual lecture that taught them about concepts and problems related to supply and demand microeconomics. They were then tested on the material either immediately, after a 12-hour period that included sleep, after 12 hours without sleep, or after one week. The test included both basic problems that they had been trained to solve, and "transfer" problems that required them to extend their knowledge to novel, but related, problems.

Performance was better for those who slept, and this was especially so for the novel, 'transfer' integration problems.

Rule-learning task also benefits from sleep

Another complex cognitive task was investigated in a study of 54 college undergraduates who were taught to play a card game for rewards of play money in which wins and losses for various card decks mimic casino gambling (the Iowa Gambling Task is typically used to assess frontal lobe function). Those who had a normal night’s sleep as part of the study drew from decks that gave them the greatest winnings four times more often than those who spent the 12-hour break awake, and they better understood the underlying rules of the game.

The students were given a brief morning or afternoon preview of the gambling task (too brief to learn the underlying rule). They returned twelve hours later (i.e., either after a normal night’s sleep, or after a day of their usual activities), when they played the full gambling task for long enough to learn the rules. Those who got to sleep between the two sessions played better and showed a better understanding of the rules when questioned.

To assure that time of day didn’t explain the different performance, two groups of 17 and 21 subjects carried out both the preview and the full task either in the morning or the evening. Time of day made no difference.

Sleep problems may be a link between perceived racism and poor health

Analysis of data from the 2006 Behavioral Risk Factor Surveillance System, involving 7,093 people in Michigan and Wisconsin, suggests that sleep deprivation may be one mediator of the oft-reported association between discrimination and poorer cognitive performance.

The survey asked the question: "Within the past 12 months when seeking health care, do you feel your experiences were worse than, the same as, or better than for people of other races?" Taking this as an index of perceived racism, and comparing it with reports of sleep disturbance (difficulty sleeping at least six nights in the past two weeks), the study found that individuals who perceived racial discrimination were significantly more likely to experience sleep difficulties, even after allowing for socioeconomic factors and depression. Risk of sleep disturbance was nearly doubled in those who perceived themselves as discriminated against, and although this was reduced after depression was taken into account, it remained significant.

Sleep problems more prevalent than expected in urban minority children

Ten families also underwent sleep monitoring at home for five to seven days. All children who completed actigraphy monitoring had shortened sleep duration, with an average sleep duration of 8 hours, significantly less than the 10 to 11 hours recommended for children in this age group.

It’s worth noting that parents consistently overestimated sleep duration. Although very aware of bedtime and wake time, parents are less aware of time spent awake during the night.

(Also note that the figures I quote are taken from the conference abstract, which differ from those quoted in the press release.)

Rocking really does help sleep

If you or your loved one is having troubles getting to sleep, you might like to note an intriguing little study involving 12 healthy males (aged 22-38, and good sleepers). The men twice took a 45-minute afternoon nap on a bed that could slowly rock. On one occasion, it was still; on the other, it rocked. Rocking brought about faster sleep, faster transition to deeper sleep, and increased slow oscillations and sleep spindles (hallmarks of deep sleep). All these results were evident in every participant.

Sleep helps long-term memory in two ways

A fruit fly study points to two dominant theories of sleep being correct. The two theories are (a) that synapses are pruned during sleep, ensuring that only the strongest connections survive (synaptic homeostasis), and (b) that memories are replayed and consolidated during sleep, so that some connections are reactivated and thus made stronger (memory consolidation).

The experiment was made possible by the development of a new strain of fruit fly that can be induced to fall asleep when temperatures rise. The synaptic homeostasis model was supported when flies were placed in socially enriched environments, then either induced to sleep or not, before being taught a courtship ritual. Those that slept developed long-term memories of the ritual, while those that didn’t sleep didn’t remember it. The memory consolidation theory was supported when flies trained using a protocol designed to give them short-term memories retained a lasting memory, if sleep was induced immediately after the training.

In other words, it seems that both pruning and replaying are important for building long-term memories.

Mouse studies identify the roots of memory impairment resulting from sleep deprivation

Sleep deprivation in known to result in increased levels of adenosine in the brain, whether fruit fly or human (caffeine blocks the effects of adenosine). New mice studies now reveal the mechanism.

Mice given a drug that blocked a particular adenosine receptor in the hippocampus (the A1 receptor) failed to show the normal memory impairment evoked by sleep deprivation (being woken halfway through their normal 12-hour sleep schedule). The same results occurred if mice were genetically engineered to lack a gene involved in the production of glial transmitters (necessary to produce adenosine).

Memory was tested by the mice being allowed to explore a box with two objects, and then returned to the box on the next day, where one of the two objects had been moved. They would normally explore the moved object more than other objects, but sleep-deprived mice don’t usually react to the change, because they don’t remember where the object had been. In both these cases, the sleep-deprived mice showed no memory impairment.

Both the drugged and genetically protected mice also showed greater synaptic plasticity in the hippocampus after being sleep deprived than the untreated group.

The two groups reveal two parts of the chemical pathway involved in sleep deprivation. The genetic engineering experiment shows that the adenosine comes from glia's release of adenosine triphosphate (ATP). The drug experiment shows that the adenosine goes to the A1 receptor in the hippocampus.

The findings provide the first evidence that astrocytic ATP and adenosine A1R activity contribute to the effects of sleep deprivation on hippocampal synaptic plasticity and hippocampus-dependent memory, and suggest a new therapeutic target to reverse the cognitive deficits induced by sleep loss.

 

Scullin M, McDaniel M, Howard D, Kudelka C. 2011. Sleep and testing promote conceptual learning of classroom materials.  Presented Tuesday, June 14, in Minneapolis, Minn., at SLEEP 2011, the 25th Anniversary Meeting of the Associated Professional Sleep Societies LLC (APSS).

[2297] Pace‐Schott, E. F., Nave G., Morgan A., & Spencer R. M. C.
(Submitted).  Sleep‐dependent modulation of affectively guided decision‐making.
Journal of Sleep Research.

Grandner MA, Hale L, Jackson NJ, Patel NP, Gooneratne N, Troxel WM. 2011. Sleep disturbance and daytime fatigue associated with perceived racial discrimination. Presented Tuesday, June 14, in Minneapolis, Minn., at SLEEP 2011, the 25th Anniversary Meeting of the Associated Professional Sleep Societies LLC (APSS).

Sheares, B.J., Dorsey, K.B., Lamm, C.I., Wei, Y., Kattan, M., Mellins, R.B. & Evans, D. 2011. Sleep Problems In Urban Minority Children May Be More Prevalent Than Previously Recognized. Presented at the ATS 2011 International Conference in Denver.

[2330] Bayer, L., Constantinescu I., Perrig S., Vienne J., Vidal P-P., Mühlethaler M., et al.
(2011).  Rocking synchronizes brain waves during a short nap.
Current Biology. 21(12), R461-R462 - R461-R462.

[2331] Donlea, J. M., Thimgan M. S., Suzuki Y., Gottschalk L., & Shaw P. J.
(2011).  Inducing Sleep by Remote Control Facilitates Memory Consolidation in Drosophila.
Science. 332(6037), 1571 - 1576.

[2287] Florian, C., Vecsey C. G., Halassa M. M., Haydon P. G., & Abel T.
(2011).  Astrocyte-Derived Adenosine and A1 Receptor Activity Contribute to Sleep Loss-Induced Deficits in Hippocampal Synaptic Plasticity and Memory in Mice.
The Journal of Neuroscience. 31(19), 6956 - 6962.

Sleep can boost classroom performance of college students http://www.eurekalert.org/pub_releases/2011-06/aaos-scb060611.php Rule-learning task also benefits from sleep http://medicalxpress.com/news/2011-05-excellent-science-based-advice.html Sleep problems may be a link between perceived racism and poor health http://medicalxpress.com/news/2011-06-problems-link-racism-poor-health.html Sleep problems more prevalent than expected in urban minority children http://medicalxpress.com/news/2011-05-problems-prevalent-urban-minority-... Rocking really does help sleep http://www.scientificamerican.com/podcast/episode.cfm?id=rocking-increas... Sleep helps long-term memory in two ways http://the-scientist.com/2011/06/23/sleep-on-it/ Mouse studies identify the roots of memory impairment resulting from sleep deprivation http://www.eurekalert.org/pub_releases/2011-05/uop-pri051711.php

Growing evidence links obesity and poorer cognitive performance. Many factors associated with obesity, such as high blood pressure, type 2 diabetes and sleep apnea, damage the brain.

A study involving109 bariatric surgery patients and 41 obese control subjects has found that the bariatric surgery patients demonstrated improved memory and concentration 12 weeks after surgery, improving from the slightly impaired range to the normal range. That of the obese controls actually declined over this period. The improvement of those who had surgery seemed to be particularly related to improved blood pressure.

Study participants will be tested one year and two years after surgery.

[2224] Gunstad, J., Strain G., Devlin M. J., Wing R., Cohen R. A., Paul R. H., et al.
(2010).  Improved memory function 12 weeks after bariatric surgery.
Surgery for Obesity and Related Diseases.

A study involving 200 older adults (70+) experiencing a stay in hospital has found that at discharge nearly a third (31.5%) had previously unrecognized low cognitive function (scoring below 25 on the MMSE if high-school-educated, or below 18 if not). This impairment had disappeared a month later for more than half (58%).The findings are consistent with previous research showing a lack of comprehension of discharge instructions, often resulting in rehospitalization.

The findings demonstrate the effects of hospitalization on seniors, and point to the need for healthcare professionals and family to offer additional support. It’s suggested that patient self-management may be better taught as an outpatient following discharge rather than at the time of hospital discharge.

Sleep disruption and stress are presumed to be significant factors in why this occurs.

A study involving 1426 long-term survivors of childhood cancer (survivors of eight different childhood cancers who were treated between 1970 and 1986) has revealed cognitive impairment in over a fifth. Those who reported problems sleeping or frequent daytime sleepiness and fatigue were three to four times more likely to have attention and memory problems.

Additionally, those who were taking antidepressants were 50% more likely to report attention problems and 70% more likely to report memory problems.

The findings emphasize the need for help in sleep hygiene for this group.

From the Whitehall II study, data involving 5431 older participants (45-69 at baseline) has revealed a significant effect of midlife sleep changes on later cognitive function. Sleep duration was assessed at one point between 1997 and 1999, and again between 2002 and 2004. A decrease in average night’s sleep from 6, 7, or 8 hours was significantly associated with poorer scores on tests of reasoning, vocabulary, and the MMSE. An increase from 7 or 8 hours (but not from 6 hours) was associated with lower scores on these, as well as on tests of phonemic and semantic fluency. Short-term verbal memory was not significantly affected. The magnitude of these effects was equivalent to a 4–7 year increase in age.

Around 8% of participants showed an increase from 7-8 hours of sleep over the five-year period (7.4% of women; 8.6% of men), while around a quarter of women and 18% of men decreased their sleep amount from 6-8 hours. About 58% of men and 50% of women reported no change in sleep duration during the study period. Some 27% of the participants were women.

The optimal amount of sleep (in terms of highest cognitive performance) was 7 hours for women, closely followed by 6 hours. For men, results were similar at 6, 7 and 8 hours.

Analysis took into account age, sex, education and occupational status. The Whitehall II study is a large, long-running study involving British civil servants. Sleep duration was assessed simply by responses to the question "How many hours of sleep do you have on an average week night?"

A very large Chinese study, involving 28,670 older adults (50-85), of whom some 72% were women, also supports an inverted U-shaped association between sleep duration and cognitive function, with 7-8 hours sleep associated with the highest scores on a delayed word recall test.

I would speculate that this finding of an effect of short-term verbal memory (in contrast to that of the Whitehall study) may reflect a group distinction in terms of education and occupation. The Whitehall study is the more homogenous (mostly white-collar), with participants probably averaging greater cognitive reserve than the community-based Chinese study. The findings suggest that memory is slower to be affected, rather than not affected.

Ferrie JE; Shipley MJ; Akbaraly TN; Marmot MG; Kivimäki M; Singh-Manoux A. Change in sleep duration and cognitive function: findings from the Whitehall II study. SLEEP 2011;34(5):565-573.

Xu L; Jiang CQ; Lam TH; Liu B; Jin YL; Zhu T; Zhang WS; Cheng KK; Thomas GN. Short or long sleep duration is associated with memory impairment in older Chinese: the Guangzhou Biobank Cohort Study. SLEEP 2011;34(5):575-580.

In a study involving 44 young adults given a rigorous memorizing task at noon and another such task at 6pm, those who took a 90-minute nap during the interval improved their ability to learn on the later task, while those who stayed awake found it harder to learn.

The degree to which the nappers were refreshed correlated with the amount of stage 2 non-REM sleep they experienced. This sleep phase is characterized by sleep spindles, which are associated with brain activity between the hippocampus and prefrontal cortex. Spindle-rich sleep occurs mostly in the second half of the night, so those who don’t get their quota of sleep are probably getting less.

The finding confirms the idea that learning ability decreases the more time you spend awake.

[2144] Mander, B. A., Santhanam S., Saletin J. M., & Walker M. P.
(2011).  Wake deterioration and sleep restoration of human learning.
Current Biology. 21(5), R183-R184 - R183-R184.

Comparison of 17 people with severe obstructive sleep apnea (OSA) with 15 age-matched controls has revealed that those with OSA had reduced gray matter in several brain regions, most particularly in the left parahippocampal gyrus and the left posterior parietal cortex, as well as the entorhinal cortex and the right superior frontal gyrus. These areas were associated with deficits in abstract reasoning and executive function. Deficits in the left posterior parietal cortex were also associated with daytime sleepiness.

Happily, however, three months of treatment with continuous positive airway pressure (CPAP), produced a significant increase in gray matter in these regions, which was associated with significant improvement in cognitive function. The researchers suggest that the hippocampus, being especially sensitive to hypoxia and innervation of small vessels, is the region most strongly and quickly affected by hypoxic episodes.

The findings point to the importance of diagnosing and treating OSA.

A study involving 48 healthy adults aged 18-39 has found that extraverts who were deprived of sleep for 22 hours after spending 12 hours in group activities performed worse on a vigilance task that did those extraverts who engaged in the same activities on their own in a private room. Introverts were relatively unaffected by the degree of prior social interaction.

The researchers suggest that social interactions are cognitively complex experiences that may lead to rapid fatigue in brain regions that regulate attention and alertness, and (more radically) that introverts may have higher levels of cortical arousal, giving them greater resistance to sleep deprivation.

Rupp TL; Killgore WDS; Balkin TJ. Socializing by day may affect performance by night: vulnerability to sleep deprivation is differentially mediated by social exposure in extraverts vs introverts. SLEEP 2010;33(11):1475-1485.

A study involving 135 adults (33-65) has found that, not only did patients with obstructive sleep apnea who were being treated with CPAP therapy outperform untreated OSA patients on an overnight picture memory task, but they outperformed controls who did not have OSA. The memory task involved being shown 20 photographs before spending the night in the sleep lab, and then having to choose the familiar photo from 20 similar pairs in the morning. CPAP therapy provides a steady stream of air through a mask that is worn during sleep.

Payne, J.D. et al. 2010. Regeneration of overnight memory consolidation ability in cpap patients. Presented at SLEEP 2010, the 24th annual meeting of the Associated Professional Sleep Societies LLC, in San Antonio, Texas.

A study involving 163 overweight children and adolescents aged 10 to 17 has revealed that moderate to severe obstructive sleep apnea was linked to both lower academic grades and behavioral concerns. None of the students with moderate to severe OSA had an "A" average, and 30% had a "C" average or lower. In contrast, roughly 15% of those without sleep-disordered breathing had an "A" average, and only about 15% had a "C" average or lower. The results remained significant after adjustment for sex, race, socioeconomic status and sleep duration on school nights. OSA was particularly associated with inattention and poor study skills in real-world situations Forty-two students had moderate to severe OSA; 58 had mild OSA; 26 students were snorers; 37 had no sleep-disordered breathing.

Beebe, D.W. et al. 2010. The association between sleep-disordered breathing, academic grades, and neurobehavioral functioning among overweight subjects during middle to late childhood. Presented at SLEEP 2010, the 24th annual meeting of the Associated Professional Sleep Societies LLC, in San Antonio, Texas.

A national study involving some 8,000 children, has revealed receptive and expressive language, phonological awareness, literacy and early math abilities were all better in 4-year-old children whose parents reported having rules about what time their child goes to bed. Having an earlier bedtime also was predictive of higher scores for most developmental measures. Recommendations are that preschool children get a minimum of 11 hours of sleep each night. These findings (which confirm earlier studies) indicate not only that lower scores on phonological awareness, literacy and early math skills are associated with getting less than this recommended amount of sleep, but that many children are not getting the recommended amount of sleep.

Gaylor, E., Wei, X. & Burnham, M.M. 2010. Associations between nighttime sleep duration and developmental outcomes in a nationally representative sample of preschool-age children. Presented at SLEEP 2010, the 24th annual meeting of the Associated Professional Sleep Societies LLC, in San Antonio, Texas.

It’s not just a matter of quantity; quality of sleep matters too. A study involving 72 adults (average age 40), whose sleep was monitored for 11 consecutive nights, has revealed that reaction times on a morning psychomotor vigilance task was significantly slower after exposure to recorded traffic noise during sleep. The slowing was directly related to the frequency and sound-pressure level of the nightly noise. Traffic noise has been identified as one cause of "environmental sleep disorder," which involves an environmental disturbance that causes a complaint of insomnia or daytime sleepiness. Other common causes include bright light and temperature extremes. The researchers also note that nighttime traffic noise may have even stronger effects on the performance of people who are more susceptible to sleep disturbances. Risk groups include children, shift workers, the elderly and people with chronic medical conditions. White noise, produced by fans, sound machines, and special applications for computers and smart phones, can be used to mask other noise.

Elmenhorst, E. et al. 2010. Nocturnal traffic noise and morning cognitive performance. Presented at SLEEP 2010, the 24th annual meeting of the Associated Professional Sleep Societies LLC, in San Antonio, Texas.

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).

http://www.eurekalert.org/pub_releases/2009-11/acoc-sat102709.php

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.

http://www.eurekalert.org/pub_releases/2009-10/aaos-aeo092309.php

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.

http://www.eurekalert.org/pub_releases/2009-10/uop-fsp102609.php

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

http://www.the-scientist.com/blog/display/55996/

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 http://www.eurekalert.org/pub_releases/2009-06/aaos-ocb052209.php).

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.

http://www.eurekalert.org/pub_releases/2009-06/aaos-is060209.php

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 http://www.eurekalert.org/pub_releases/2009-06/sfn-gph062409.php).

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.

http://www.eurekalert.org/pub_releases/2009-06/aaos-oal060209.php

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.

http://www.eurekalert.org/pub_releases/2009-03/aaos-csp022709.php

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.

http://www.eurekalert.org/pub_releases/2008-12/uoc--tsa120308.php

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.

http://www.eurekalert.org/pub_releases/2008-10/ncsu-lsl101308.php

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.

http://www.eurekalert.org/pub_releases/2008-08/sfn-osn081808.php

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.

http://www.eurekalert.org/pub_releases/2008-06/uoc--mll060608.php

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).

http://www.eurekalert.org/pub_releases/2008-06/aaos-iit050708.php

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.

http://www.eurekalert.org/pub_releases/2008-05/ats-gtc051308.php

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.

http://www.eurekalert.org/pub_releases/2008-02/aaos-fdo012808.php

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.

http://www.eurekalert.org/pub_releases/2007-09/aaos-jsl082407.php

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.

http://www.eurekalert.org/pub_releases/2007-07/aaon-oww071007.php

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.

http://www.eurekalert.org/pub_releases/2007-02/sfri-csp013107.php

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.

http://news.bbc.co.uk/2/hi/health/6347043.stm

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.

http://www.eurekalert.org/pub_releases/2006-12/acoc-mia120606.php

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 http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.0030301

http://www.eurekalert.org/pub_releases/2006-08/jhmi-csa081506.php

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.

http://www.eurekalert.org/pub_releases/2006-01/uoca-mgm121905.php

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.

http://www.eurekalert.org/pub_releases/2006-01/aps-lsu010506.php

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.

http://www.eurekalert.org/pub_releases/2004-10/nhla-bpd100604.php

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.

http://www.eurekalert.org/pub_releases/2004-05/cwru-mrr050404.php

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.

http://www.eurekalert.org/pub_releases/2003-11/sfn-sfb_1111003.php

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.

http://www.eurekalert.org/pub_releases/2008-10/aaos-lts092908.php

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