News Topic TBI
About these topic collections
I’ve been reporting on memory research for over ten years and these topic pages are simply collections of all the news items I have made on a particular topic. They do not pretend to be in any way exhaustive! I cover far too many areas within memory to come anywhere approaching that. What I aim to do is provide breadth, rather than depth. Outside my own area of cognitive psychology, it is difficult to know how much weight to give to any study (I urge you to read my blog post on what constitutes scientific evidence). That (among other reasons) is why my approach in my news reporting is based predominantly on replication and consistency. It's about the aggregate. So here is the aggregate of those reports I have at one point considered of sufficient interest to discuss. If you know of any research you would like to add to the collection, feel free to write about it in a comment (please provide a reference).
Studies linking head trauma with increased risk and earlier age of onset for Alzheimer's disease have yielded contradictory results. Now a population-based study involving 448 healthy older adults (70+) and 141 seniors with mild cognitive impairment has found that a history of head trauma was associated with higher levels of amyloid-beta plaques (a marker for Alzheimer’s) in those with MCI, but not in the cognitively normal. Similar rates of self-reported head trauma were found in the two groups (17% and 18%, respectively).
 Head trauma and in vivo measures of amyloid and neurodegeneration in a population-based study. Neurology. 82(1), 70 - 76.(2014).
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.
A study involving 67 college football players has found that a protein biomarker for traumatic brain injury (S100B) was present in varying degrees in the blood samples of all the players after every game, even though none of them suffered a concussion. This demonstrates that even the most routine hits have some impact on the blood-brain barrier and possibly the brain itself.
Moreover, this protein is viewed as an enemy by the body, which reacts by building antibodies. Some of these antibodies pass through the damaged blood-brain barrier to attack the neurons that produced the protein. It’s suggested that the brain degeneration observed among professional football players could result from an out-of-control immune response, with the blood-brain barrier repeatedly opening during the football season, leaving the brain open to a continuous autoimmune-type attack.
Players with the most head hits had the highest S100B levels and elevated levels of autoimmune antibodies.
 Consequences of Repeated Blood-Brain Barrier Disruption in Football Players. PLoS ONE. 8(3),(2013).
I’ve talked before about how even mild head injuries can have serious consequences, and in recent years we’ve seen growing awareness of the long-term dangers of sports’ concussions (especially for young people). This has been followed by a number of initiatives to help protect athletes. However, while encouraging, they may still be under-estimating the problem. Two recent studies, involving high school athletes who had experienced concussions, point to quite subtle impairment lasting for longer than expected.
In one study, 20 concussed adolescents were tested on their attention and executive function within 72 hours post injury, and then again at one week, two weeks, one month, and two months post injury. Compared with matched controls, they had a significantly greater switch cost on the Task-Switching Test and a significantly greater reaction time for the Attentional Network Test conflict effect component, with this lasting up to two months after injury.
The results suggest that longer recovery periods than the standard 7-10 days may be warranted, given that the slower reaction times (although only a matter of milliseconds) might make further injury more likely.
In another study, 54 adolescent athletes who had been concussed but who reported being symptom-free and had returned to baseline neurocognitive-test levels, were given, further testing. This revealed that over a quarter of them (27.7%) showed cognitive impairment following moderate physical exertion (15 to 25 minutes on a treadmill, elliptical, or stationary bicycle). These athletes scored significantly lower on verbal and visual memory, although processing speed and reaction was not affected (suggesting that tests focusing mainly on these latter abilities are insufficient).
The group affected did not differ from the rest in terms of symptoms or concussion history.
The findings suggest that computerized neurocognitive testing following moderate exertion should be part of the standard procedure when making return-to-play decisions.
 Effects of Concussion on Attention and Executive Function in Adolescents. Medicine & Science in Sports & Exercise.(2012).
 Post-exertion neurocognitive test failure among student-athletes following concussion. Brain Injury. 27(1), 103 - 113.(2013).
By using brain scans from 152 Vietnam veterans with a variety of combat-related brain injuries, researchers claim to have mapped the neural basis of general intelligence and emotional intelligence.
There was significant overlap between general intelligence and emotional intelligence, both in behavioral measures and brain activity. Higher scores on general intelligence tests and personality reliably predicted higher performance on measures of emotional intelligence, and many of the same brain regions (in the frontal and parietal cortices) were found to be important to both.
More specifically, impairments in emotional intelligence were associated with selective damage to a network containing the extrastriate body area (involved in perceiving the form of other human bodies), the left posterior superior temporal sulcus (helps interpret body movement in terms of intentions), left temporo-parietal junction (helps work out other person’s mental state), and left orbitofrontal cortex (supports emotional empathy). A number of associated major white matter tracts were also part of the network.
Two of the components of general intelligence were strong contributors to emotional intelligence: verbal comprehension/crystallized intelligence, and processing speed. Verbal impairment was unsurprisingly associated with selective damage to the language network, which showed some overlap with the network underlying emotional intelligence. Similarly, damage to the fronto-parietal network linked to deficits in processing speed also overlapped in places with the emotional intelligence network.
Only one of the ‘big five’ personality traits contributed to the prediction of emotional intelligence — conscientiousness. Impairments in conscientiousness were associated with damage to brain regions widely implicated in social information processing, of which two areas (left orbitofrontal cortex and left temporo-parietal junction) were also involved in impaired emotional intelligence, suggesting where these two attributes might be connected (ability to predict and understand another’s emotions).
It’s interesting (and consistent with the growing emphasis on connectivity rather than the more simplistic focus on specific regions) that emotional intelligence was so affected by damage to white matter tracts. The central role of the orbitofrontal cortex is also intriguing – there’s been growing evidence in recent years of the importance of this region in emotional and social processing, and it’s worth noting that it’s in the right place to integrate sensory and bodily sensation information and pass that onto decision-making systems.
All of this is to say that emotional intelligence depends on social information processing and general intelligence. Traditionally, general intelligence has been thought to be distinct from social and emotional intelligence. But humans are fundamentally social animals, and – contra the message of the Enlightenment, that we have taken so much to heart – it has become increasingly clear that emotions and reason are inextricably entwined. It is not, therefore, all that surprising that general and emotional intelligence might be interdependent. It is more surprising that conscientiousness might be rooted in your degree of social empathy.
It’s also worth noting that ‘emotional intelligence’ is not simply a trendy concept – a pop quiz question regarding whether you ‘have a high EQ’ (or not), but that it can, if impaired, produce very real problems in everyday life.
Emotional intelligence was measured by the Mayer, Salovey, Caruso Emotional Intelligence Test (MSCEIT), general IQ by the Wechsler Adult Intelligence Scale, and personality by the Neuroticism-Extroversion-Openness Inventory.
 Distributed neural system for emotional intelligence revealed by lesion mapping. Social Cognitive and Affective Neuroscience.(2012).
Sometime ago, I reported on a study showing that older adults could improve their memory for a future task (remembering to regularly test their blood sugar) by picturing themselves going through the process. Imagination has been shown to be a useful strategy in improving memory (and also motor skills). A new study extends and confirms previous findings, by testing free recall and comparing self-imagination to more traditional strategies.
The study involved 15 patients with acquired brain injury who had impaired memory and 15 healthy controls. Participants memorized five lists of 24 adjectives that described personality traits, using a different strategy for each list. The five strategies were:
For both groups, self-imagination produced the highest rates of free recall of the list (an average of 9.3 for the memory-impaired, compared to 3.2 using the baseline strategy; 8.1 vs 3.2 for the controls — note that the controls were given all 24 items in one list, while the memory-impaired were given 4 lists of 6 items).
Additionally, those with impaired memory did better using semantic self-referential processing than episodic self-referential processing (7.3 vs 5.7). In contrast, the controls did much the same in both conditions. This adds to the evidence that patients with brain injury often have a particular problem with episodic memory (knowledge about specific events). Episodic memory is also particularly affected in Alzheimer’s, as well as in normal aging and depression.
It’s also worth noting that all the strategies that involved the self were more effective than the two strategies that didn’t, for both groups (also, semantic elaboration was better than the baseline strategy).
The researchers suggest self-imagination (and semantic self-referential processing) might be of particular benefit for memory-impaired patients, by encouraging them to use information they can more easily access (information about their own personality traits, identity roles, and lifetime periods — what is termed the self-schema), and that future research should explore ways in which self-imagination could be used to support everyday memory tasks, such as learning new skills and remembering recent events.
 Imagining a Better Memory Self-Imagination in Memory-Impaired Patients. Clinical Psychological Science.(2012).
Full text available at http://cpx.sagepub.com/content/early/2012/10/02/2167702612456464
Genetic analysis of 9,232 older adults (average age 67; range 56-84) has implicated four genes in how fast your hippocampus shrinks with age (rs7294919 at 12q24, rs17178006 at 12q14, rs6741949 at 2q24, rs7852872 at 9p33). The first of these (implicated in cell death) showed a particularly strong link to a reduced hippocampus volume — with average consequence being a hippocampus of the same size as that of a person 4-5 years older.
Faster atrophy in this crucial brain region would increase people’s risk of Alzheimer’s and cognitive decline, by reducing their cognitive reserve. Reduced hippocampal volume is also associated with schizophrenia, major depression, and some forms of epilepsy.
In addition to cell death, the genes linked to this faster atrophy are involved in oxidative stress, ubiquitination, diabetes, embryonic development and neuronal migration.
A younger cohort, of 7,794 normal and cognitively compromised people with an average age of 40, showed that these suspect gene variants were also linked to smaller hippocampus volume in this age group. A third cohort, comprised of 1,563 primarily older people, showed a significant association between the ASTN2 variant (linked to neuronal migration) and faster memory loss.
In another analysis, researchers looked at intracranial volume and brain volume in 8,175 elderly. While they found no genetic associations for brain volume (although there was one suggestive association), they did discover that intracranial volume (the space occupied by the fully developed brain within the skull — this remains unchanged with age, reflecting brain size at full maturity) was significantly associated with two gene variants (at loci rs4273712, on chromosome 6q22, and rs9915547, on 17q21). These associations were replicated in a different sample of 1,752 older adults. One of these genes is already known to play a unique evolutionary role in human development.
A meta-analysis of seven genome-wide association studies, involving 10,768 infants (average age 14.5 months), found two loci robustly associated with head circumference in infancy (rs7980687 on chromosome 12q24 and rs1042725 on chromosome 12q15). These loci have previously been associated with adult height, but these effects on infant head circumference were largely independent of height. A third variant (rs11655470 on chromosome 17q21 — note that this is the same chromosome implicated in the study of older adults) showed suggestive evidence of association with head circumference; this chromosome has also been implicated in Parkinson's disease and other neurodegenerative diseases.
Previous research has found an association between head size in infancy and later development of Alzheimer’s. It has been thought that this may have to do with cognitive reserve.
Interestingly, the analyses also revealed that a variant in a gene called HMGA2 (rs10784502 on 12q14.3) affected intelligence as well as brain size.
Why ‘Alzheimer’s gene’ increases Alzheimer’s risk
Investigation into the so-called ‘Alzheimer’s gene’ ApoE4 (those who carry two copies of this variant have roughly eight to 10 times the risk of getting Alzheimer’s disease) has found that ApoE4 causes an increase in cyclophilin A, which in turn causes a breakdown of the cells lining the blood vessels. Blood vessels become leaky, making it more likely that toxic substances will leak into the brain.
The study found that mice carrying the ApoE4 gene had five times as much cyclophilin A as normal, in cells crucial to maintaining the integrity of the blood-brain barrier. Blocking the action of cyclophilin A brought blood flow back to normal and reduced the leakage of toxic substances by 80%.
The finding is in keeping with the idea that vascular problems are at the heart of Alzheimer’s disease — although it should not be assumed from that, that other problems (such as amyloid-beta plaques and tau tangles) are not also important. However, one thing that does seem clear now is that there is not one single pathway to Alzheimer’s. This research suggests a possible treatment approach for those carrying this risky gene variant.
Note also that this gene variant is not only associated with Alzheimer’s risk, but also Down’s syndrome dementia, poor outcome following TBI, and age-related cognitive decline.
On which note, I’d like to point out recent findings from the long-running Nurses' Health Study, involving 16,514 older women (70-81), that suggest that effects of postmenopausal hormone therapy for cognition may depend on apolipoprotein E (APOE) status, with the fastest rate of decline being observed among HT users who carried the APOe4 variant (in general HT was associated with poorer cognitive performance).
It’s also interesting to note another recent finding: that intracranial volume modifies the effect of apoE4 and white matter lesions on dementia risk. The study, involving 104 demented and 135 nondemented 85-year-olds, found that smaller intracranial volume increased the risk of dementia, Alzheimer's disease, and vascular dementia in participants with white matter lesions. However, white matter lesions were not associated with increased dementia risk in those with the largest intracranial volume. But intracranial volume did not modify dementia risk in those with the apoE4 gene.
More genes involved in Alzheimer’s
More genome-wide association studies of Alzheimer's disease have now identified variants in BIN1, CLU, CR1 and PICALM genes that increase Alzheimer’s risk, although it is not yet known how these gene variants affect risk (the present study ruled out effects on the two biomarkers, amyloid-beta 42 and phosphorylated tau).
Same genes linked to early- and late-onset Alzheimer's
Traditionally, we’ve made a distinction between early-onset Alzheimer's disease, which is thought to be inherited, and the more common late-onset Alzheimer’s. New findings, however, suggest we should re-think that distinction. While the genetic case for early-onset might seem to be stronger, sporadic (non-familial) cases do occur, and familial cases occur with late-onset.
New DNA sequencing techniques applied to the APP (amyloid precursor protein) gene, and the PSEN1 and PSEN2 (presenilin) genes (the three genes linked to early-onset Alzheimer's) has found that rare variants in these genes are more common in families where four or more members were affected with late-onset Alzheimer’s, compared to normal individuals. Additionally, mutations in the MAPT (microtubule associated protein tau) gene and GRN (progranulin) gene (both linked to frontotemporal dementia) were also found in some Alzheimer's patients, suggesting they had been incorrectly diagnosed as having Alzheimer's disease when they instead had frontotemporal dementia.
Of the 439 patients in which at least four individuals per family had been diagnosed with Alzheimer's disease, rare variants in the 3 Alzheimer's-related genes were found in 60 (13.7%) of them. While not all of these variants are known to be pathogenic, the frequency of mutations in these genes is significantly higher than it is in the general population.
The researchers estimate that about 5% of those with late-onset Alzheimer's disease have changes in these genes. They suggest that, at least in some cases, the same causes may underlie both early- and late-onset disease. The difference being that those that develop it later have more protective factors.
Another gene identified in early-onset Alzheimer's
A study of the genes from 130 families suffering from early-onset Alzheimer's disease has found that 116 had mutations on genes already known to be involved (APP, PSEN1, PSEN2 — see below for some older reports on these genes), while five of the other 14 families all showed mutations on a new gene: SORL1.
I say ‘new gene’ because it hasn’t been implicated in early-onset Alzheimer’s before. However, it has been implicated in the more common late-onset Alzheimer’s, and last year a study reported that the gene was associated with differences in hippocampal volume in young, healthy adults.
The finding, then, provides more support for the idea that some cases of early-onset and late-onset Alzheimer’s have the same causes.
The SORL1 gene codes for a protein involved in the production of the beta-amyloid peptide, and the mutations seen in this study appear to cause an under-expression of SORL1, resulting in an increase in the production of the beta-amyloid peptide. Such mutations were not found in the 1500 ethnicity-matched controls.
Older news reports on these other early-onset genes (brought over from the old website):
New genetic cause of Alzheimer's disease
Amyloid protein originates when it is cut by enzymes from a larger precursor protein. In very rare cases, mutations appear in the amyloid precursor protein (APP), causing it to change shape and be cut differently. The amyloid protein that is formed now has different characteristics, causing it to begin to stick together and precipitate as amyloid plaques. A genetic study of Alzheimer's patients younger than 70 has found genetic variations in the promoter that increases the gene expression and thus the formation of the amyloid precursor protein. The higher the expression (up to 150% as in Down syndrome), the younger the patient (starting between 50 and 60 years of age). Thus, the amount of amyloid precursor protein is a genetic risk factor for Alzheimer's disease.
Theuns, J. et al. 2006. Promoter Mutations That Increase Amyloid Precursor-Protein Expression Are Associated with Alzheimer Disease. American Journal of Human Genetics, 78, 936-946.
Evidence that Alzheimer's protein switches on genes
Amyloid b-protein precursor (APP) is snipped apart by enzymes to produce three protein fragments. Two fragments remain outside the cell and one stays inside. When APP is produced in excessive quantities, one of the cleaved segments that remains outside the cell, called the amyloid b-peptides, clumps together to form amyloid plaques that kill brain cells and may lead to the development of Alzheimer’s disease. New research indicates that the short "tail" segment of APP that is trapped inside the cell might also contribute to Alzheimer’s disease, through a process called transcriptional activation - switching on genes within the cell. Researchers speculate that creation of amyloid plaque is a byproduct of a misregulation in normal APP processing.
 A Transcriptively Active Complex of APP with Fe65 and Histone Acetyltransferase Tip60. Science. 293(5527), 115 - 120.(2001).
Inactivation of Alzheimer's genes in mice causes dementia and brain degeneration
Mutations in two related genes known as presenilins are the major cause of early onset, inherited forms of Alzheimer's disease, but how these mutations cause the disease has not been clear. Since presenilins are involved in the production of amyloid peptides (the major components of amyloid plaques), it was thought that such mutations might cause Alzheimer’s by increasing brain levels of amyloid peptides. Accordingly, much effort has gone into identifying compounds that could block presenilin function. Now, however, genetic engineering in mice has revealed that deletion of these genes causes memory loss and gradual death of nerve cells in the mouse brain, demonstrating that the protein products of these genes are essential for normal learning, memory and nerve cell survival.
Saura, C.A., Choi, S-Y., Beglopoulos, V., Malkani, S., Zhang, D., Shankaranarayana Rao, B.S., Chattarji, S., Kelleher, R.J.III, Kandel, E.R., Duff, K., Kirkwood, A. & Shen, J. 2004. Loss of Presenilin Function Causes Impairments of Memory and Synaptic Plasticity Followed by Age-Dependent Neurodegeneration. Neuron, 42 (1), 23-36.
 Common variants at 12q14 and 12q24 are associated with hippocampal volume. Nature Genetics. 44(5), 545 - 551.(2012).
 Common variants at 12q15 and 12q24 are associated with infant head circumference. Nature Genetics. 44(5), 532 - 538.(2012).
 Common variants at 6q22 and 17q21 are associated with intracranial volume. Nature Genetics. 44(5), 539 - 544.(2012).
 Identification of common variants associated with human hippocampal and intracranial volumes. Nature Genetics. 44(5), 552 - 561.(2012).
Postmenopausal hormone therapy, timing of initiation, APOE and cognitive decline. Neurobiology of Aging. 33(7), 1129 - 1137.(2012).
Head size may modify the impact of white matter lesions on dementia. Neurobiology of Aging. 33(7), 1186 - 1193.(2012).
 Rare Variants in APP, PSEN1 and PSEN2 Increase Risk for AD in Late-Onset Alzheimer's Disease Families. PLoS ONE. 7(2), e31039 - e31039.(2012).
Full text available at http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0031039
 High frequency of potentially pathogenic SORL1 mutations in autosomal dominant early-onset Alzheimer disease. Molecular Psychiatry.(2012).
The Alzheimer's associated 5′ region of the SORL1 gene cis regulates SORL1 transcripts expression. Neurobiology of Aging. 33(7), 1485.e1-1485.e8 - 1485.e1-1485.e8(2012).
Why ‘Alzheimer’s gene’ increases Alzheimer’s risk: http://www.futurity.org/health-medicine/alzheimers-gene-opens-floodgate-in-brain/
More genes involved in Alzheimer’s: Full text available at http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0015918
Same genes linked to early- and late-onset Alzheimer's: http://www.eurekalert.org/pub_releases/2012-02/wuso-sgl020112.php
Another gene identified in early-onset Alzheimer's: http://www.eurekalert.org/pub_releases/2012-04/ind-ang040412.php
I recently discussed some of the implications of head injuries and how even mild concussions can have serious and long-term consequences. A follow-up study looking at the effects of childhood traumatic brain injury ten years after the event has found that even those with mild TBI showed some measurable effects, while those with severe TBI had markedly poorer performance on a number of cognitive measures.
The study involved 40 children who were admitted to hospital with TBI in early childhood (between 2 to 7 years; average just under 5), and 16 healthy controls. The children’s cognitive functions were assessed at the time of accident, and again at 12 and 30 months and 10 years later. Of the 40 with TBIs, 7 had mild injuries, 20 had moderate, and 13 severe.
Unsurprisingly, children with severe TBI had the poorest outcomes. This group was significantly poorer (compared to controls) on full scale IQ; performance IQ; verbal IQ; verbal comprehension; perceptual organization, processing speed. Those who had moderate TBI were significantly poorer on full scale IQ and verbal comprehension only, and those with mild TBI performed more poorly than the controls on verbal comprehension only. Note the size of these effects: the average scores of the group with severe TBI were 18-26 points lower than the control group. In comparison, those with moderate TBI were around 10 points lower on the two significant measures.
These findings are in contrast to research involving adults and older children, where IQ tends to remain intact.
They also contradict the belief that young brains have greater ability to ‘bounce back’ from injury.
Interestingly, the recovery trajectory wasn’t significantly affected by severity of injury — all the groups followed a similar pattern and they all tended to plateau from 5 to 10 years after injury. In general, the findings paint a picture of a long period of disrupted development immediately after the injury, lasting perhaps as long as 30 months, before the brain has recovered sufficiently to progress relatively normally. In other words, intervention may be helpful even years after the injury.
One weakness in the study is the small number of mild TBI cases. It should also be noted that the IQ of the control group was surprisingly high (113). However, given that they had similar IQ levels to the TBI groups prior to injury, it is possible that this reflects a practice effect (but remember that all groups got the same amount of practice).
One thing I wonder about, given recent research pointing to the value of schooling in raising IQ, is the extent to which some of this is due to loss of education that may have resulted from severe injury.
Full text available at http://pediatrics.aappublications.org/content/early/2012/01/18/peds.2011...
American football has been in the news a lot in recent years, as evidence has accumulated as to the brain damage incurred by professional footballers. But American football is a high-impact sport. Soccer is quite different. And yet the latest research reveals that even something as apparently unexceptional as bouncing a ball off your forehead can cause damage to your brain, if done often enough.
Brain scans on 32 amateur soccer players (average age 31) have revealed that those who estimated heading the ball more than 1,000-1,500 times in the past year had damage to white matter similar to that seen in patients with concussion.
Six brain regions were seen to be affected: one in the frontal lobe and five in the temporo-occipital cortex. These regions are involved in attention, memory, executive functioning and higher-order visual functions. The number of headings (obviously very rough estimates, based presumably on individuals’ estimates of how often they play and how often they head the ball on average during a game) needed to produce measurable decreases in the white matter integrity varied per region. In four of temporo-occipital regions, the threshold number was around 1500; in the fifth it was only 1000; in the frontal lobe, it was 1300.
Those with the highest annual heading frequency also performed worse on tests of verbal memory and psychomotor speed (activities that require mind-body coordination, like throwing a ball).
This is only a small study and clearly more research is required, but the findings indicate that we should lower our ideas of what constitutes ‘harm’ to the brain — if repetition is frequent enough, even mild knocks can cause damage. This adds to the evidence I discussed in a recent blog post, that even mild concussions can produce long-lasting trauma to the brain, and it is important to give your brain time to repair itself.
At the moment we can only speculate on the effect such repetition might have to the vulnerable brains of children.
The researchers suggest that heading should be monitored to prevent players exceeding unsafe exposure thresholds.
Kim, N., Zimmerman, M., Lipton, R., Stewart, W., Gulko, E., Lipton, M. & Branch, C. 2011. PhD Making Soccer Safer for the Brain: DTI-defined Exposure Thresholds for White Matter Injury Due to Soccer Heading. Presented November 30 at the annual meeting of the Radiological Society of North America (RSNA) in Chicago.
Sleep apnea linked to later dementia
A study involving 298 older women with sleep problems found that those who had disordered breathing (such as sleep apnea) were significantly more likely to develop dementia or mild cognitive impairment.
Around a third of the women (average age 82) had disordered breathing (slowing down or stopping breathing during sleep and often having to gasp to catch up). None showed signs of cognitive impairment at the time of the sleep testing. When re-tested some five years later, 45% of those who had disordered breathing had developed dementia or MCI, compared with 31% of those with no breathing irregularities.
Those whose sleep irregularities had been particularly severe (15 or more breathing stoppages per hour and more than 7% of sleep time not breathing) during the earlier part of the study were nearly twice as likely as those without breathing problems to develop dementia or MCI. Other measures of sleep quality — waking after sleep onset, sleep fragmentation, sleep duration — were not associated with cognitive impairment.
The finding adds to the evidence for the importance of treating sleep apnea. Previous research has found that CPAP treatment effectively counteracts cognitive impairment caused by sleep apnea.
Brain injury raises dementia risk
Analysis of medical records on 281,540 U.S. military veterans aged at least 55 at the beginning of the study has found that over the next seven years those who had at one time suffered a traumatic brain injury were more than twice as likely to develop dementia than those who had not suffered such an injury. Around 1.7% (4,902) had incurred a traumatic brain injury, in many cases during the Vietnam War, and over 15% of these developed dementia. In contradiction of the prevailing belief that only moderate or severe brain injuries predispose people to dementia, severity of the injury made no difference.
Injuries due to strokes were weeded out of the study.
In another study, following up on nearly 4,000 retired National Football League players surveyed in 2001, 35% appeared to have significant cognitive problems (as assessed by questionnaire). When 41 of them were tested, they were found to have mild cognitive impairment that resembled a comparison group of much older patients from the general population.
The findings are a reminder of the importance of treating even mild head injuries, and of following a regime designed to mitigate damage: exercising, eating a healthy diet, reducing stress, and so on.
 Sleep-Disordered Breathing, Hypoxia, and Risk of Mild Cognitive Impairment and Dementia in Older Women. JAMA: The Journal of the American Medical Association. 306(6), 613 - 619.(2011).
The brain injury studies were reported in July at the Alzheimer's Association International Conference in France. http://www.alz.org/aaic/
A study involving 38 people suffering from mild traumatic brain injury (TBI) has found that those receiving acupressure treatments from trained experts (eight treatments over 4 weeks) scored significantly better on tests of working memory compared to those who received treatments from the same experts on places on the body that are not considered to be acupressure points.
Acupressure involves the practitioner using his fingertips to stimulate particular points on a person's body. The acupressure treatment type used in the study was Jin Shin. This treatment can be taught to family and friends of those with TBI and can even be used as a self-treatment, making it a good candidate for an adjunct treatment for TBI.
 Acupressure as a Non-Pharmacological Intervention for Traumatic Brain Injury (TBI). Journal of Neurotrauma. 28(1), 21 - 34.(2011).
Following indications that the curry spice curcumin (the active ingredient in turmeric) may help protect brain cells from damage, two new studies have been testing a compound called CNB-001, derived from curcumin.
The first (rabbit) study found that CNB-001 is at least as effective as the only existing drug used to treat stroke (TPA), without the unwanted side-effect of reducing clotting in the blood vessels of the brain.
The second study found that CNB-001 dramatically reversed the behavioral deficits in both locomotion and memory in brain-injured rats. As with stroke, CNB-001 was again found to maintain the critical signaling pathways required for nerve cell survival, as well as the connections between nerve cells that are lost with the injury.
At present, there is no treatment for TBI, and only one FDA-approved drug for ischemic stroke
 Delayed treatment with a novel neurotrophic compound reduces behavioral deficits in rabbit ischemic stroke. Journal of Neurochemistry. 116(1), 122 - 131.(2011).
When stroke or brain injury damages a part of the brain controlling movement or sensation or language, other parts of the brain can learn to compensate for this damage. It’s been thought that this is a case of one region taking over the lost function. Two new studies show us the story is not so simple, and help us understand the limits of this plasticity.
In the first study, six stroke patients who have lost partial function in their prefrontal cortex, and six controls, were briefly shown a series of pictures to test the ability to remember images for a brief time (visual working memory) while electrodes recorded their EEGs. When the images were shown to the eye connected to the damaged hemisphere, the intact prefrontal cortex (that is, the one not in the hemisphere directly receiving that visual input) responded within 300 to 600 milliseconds.
Visual working memory involves a network of brain regions, of which the prefrontal cortex is one important element, and the basal ganglia, deep within the brain, are another. In the second study, the researchers extended the experiment to patients with damage not only to the prefrontal cortex, but also to the basal ganglia. Those with basal ganglia damage had problems with visual working memory no matter which part of the visual field was shown the image.
In other words, basal ganglia lesions caused a more broad network deficit, while prefrontal cortex lesions resulted in a more limited, and recoverable, deficit. The findings help us understand the different roles these brain regions play in attention, and emphasize how memory and attention are held in networks. They also show us that the plasticity compensating for brain damage is more dynamic and flexible than we realized, with intact regions stepping in on a case by case basis, very quickly, but only when the usual region fails.
 Dynamic Neuroplasticity after Human Prefrontal Cortex Damage. Neuron. 68(3), 401 - 408.(2010).
 Prefrontal cortex and basal ganglia contributions to visual working memory. Proceedings of the National Academy of Sciences. 107(42), 18167 - 18172.(2010).
A rat study using powerful imaging techniques has revealed how an injured brain continues to change long after the original trauma. Widespread decreases in brain functioning over a period of months were seen in specific brain regions, in particular the hippocampus, amygdala, and ipsilateral cortex, even when these were remote from the site of direct trauma and unaccompanied by signs of injury.
The findings indicate that there is a time window during which intervention could reduce these processes and protect against some of the disabling consequences of TBI.
 Progressive Metabolic and Structural Cerebral Perturbations After Traumatic Brain Injury: An In Vivo Imaging Study in the Rat. J Nucl Med. 51(11), 1788 - 1795.(2010).
Monitoring of 11 football players at a high school in Indiana, who wore helmets equipped with sensors that recorded impart, has revealed the problem of head injuries is deeper than was thought. Brain scans and cognitive tests, in addition to the impact data, found that some players who hadn't been diagnosed with concussions nevertheless had developed changes in brain function, correlated with cognitive impairment. The findings point to the dangers of repeated impact, regardless of whether consciousness is lost.
The research is ongoing, and aims to determine how many blows it takes to cause impairment, and whether players accumulate damage over several sessions, or recover. The work to date suggests that those who developed impairment in the absence of concussion received a large number of blows primarily to the top and front of the head. This is just above the dorsolateral prefrontal cortex, which showed changes in activation. Visual working memory was the function principally affected.
Researchers are also working to create a helmet that reduces the cumulative effect of impacts.
 Functionally-Detected Cognitive Impairment in High School Football Players Without Clinically-Diagnosed Concussion. Journal of Neurotrauma. 101001044014052 - 101001044014052.(2010).
A number of studies in recent years have revealed the amazing ability of the human brain to compensate for damage down to its part. In the latest of these, it’s been found that loss of the amygdala doesn’t have to mean that new memories will be void of emotion. Instead, it appears, a region called the bed nuclei can step in to take its place. The bed nuclei are slower to process information than the amygdala, and in normal circumstances are inhibited by the amygdala. The study looked specifically at fear conditioning, for which the amygdala has been considered crucial.
The finding offers the hope that therapies to promote compensatory shifts in function might help those who have suffered damage to parts of their brain.
 Compensation in the neural circuitry of fear conditioning awakens learning circuits in the bed nuclei of the stria terminalis. Proceedings of the National Academy of Sciences. 107(33), 14881 - 14886.(2010).
Older news items (pre-2010) brought over from the old website
Nerve-cell transplants help brain-damaged rats recover lost ability to learn
After destroying neurons in the subiculum of 48 adult rats, some were given hippocampal cells taken from newborn transgenic mice. On spatial memory tests two months later, the rats given cell transplants performed as well as rats which had not had their subiculums damaged; however, those without transplants had significantly impaired performance. The new cells were found to have mainly settled in the dentate gyrus, where they appeared to promote the secretion of two types of growth factors, namely BDNF and basic fibroblast growth factor (bFGF).
Rekha, J. et al. 2009. Transplantation of hippocampal cell lines restore spatial learning in rats with ventral subicular lesions. Behavioral Neuroscience, 123(6), 1197-1217.
Amino acid diet helps brain-injured mice
In a study in which brain-injured mice received a cocktail of three branched chain amino acids (BCAAs), specifically leucine, isoleucine and valine, in their drinking water, those who received the cocktail showed normal learning ability and normal activity in the hippocampus. BCAAs are crucial precursors of two neurotransmitters—glutamate and GABA, which function together to maintain an appropriate balance of brain activity. Previously, it’s been found that people with severe brain injuries showed mild functional improvements after receiving BCAAs through an intravenous line. It’s suggested that receiving the BCAAs as a dietary supplement could have a more sustained, measured benefit than that seen when patients receive BCAAs intravenously, in which the large IV dose may flood brain receptors and have more limited benefits.
 Dietary branched chain amino acids ameliorate injury-induced cognitive impairment. Proceedings of the National Academy of Sciences. 107(1), 366 - 371.(2010).
Greater dementia risk in former N.F.L. players
A study commissioned by the National Football League reports that Alzheimer’s disease or similar memory-related diseases appear to have been diagnosed in the league’s former players vastly more often than in the national population: five times the national average among those 50 and older (6.1%)and 19 times for those aged 30 through 49. The findings are consistent with several recent studies regarding N.F.L. players and the effects of their occupational head injuries. The study involved a phone survey of 1,063 retired players (from an original random list of 1,625), who were asked questions derived from the standard National Health Interview Survey. Some health issues were reported at higher than the population rate (sleep apnea and elevated cholesterol — both risk factors for cognitive problems).
Stroke patients regain sight after intensive brain training
In a surprising and exciting finding, stroke victims left partially blind have been trained to use undamaged parts of their brains to improve their vision. The training program, involving an hour a day for at least nine months, forced them to process visual signals with parts of their brain that had not been damaged by the stroke. The seven patients in the study ranged in age from their 30s to 80s, and had suffered a stroke between eight months and three-and-a-half years previously. Impaired vision is a very common result of a stroke.
 Perceptual Relearning of Complex Visual Motion after V1 Damage in Humans. J. Neurosci.. 29(13), 3981 - 3991.(2009).
Patients who recover well from head injury 'work harder' to perform at same level as healthy people
People who make a full recovery from head injury often report "mental fatigue" and feeling "not quite the same" – even though they scored well on standard cognitive tests. Now brain imaging reveals that even with recovered head injury patients performing as well as matched controls on a series of working memory tests, their brains were working harder — specifically, showing more activity in regions of the prefrontal cortex and posterior cortices. All the patients had diffuse axonal injury, the most common consequence of head injuries resulting from motor vehicle accidents, falls, combat-related blast injuries, and other situations where the brain is rattled violently inside the skull causing widespread disconnection of brain cells.
 Augmented neural activity during executive control processing following diffuse axonal injury. Neurology. 71(11), 812 - 818.(2008).
Feed TBI patients early and well
Analysis of the results of 797 comatose brain trauma patients treated at 21 trauma centers in New York over six years has found that patients who did not get fed within five or seven days were two-fold and four-fold more likely to die in the two week period following initial trauma. The amount of nutrition in the first 5 days was related to death; every 10-kcal/kg decrease in caloric intake was associated with a 30–40% increase in mortality rates. The findings overturn current guidelines for TBI patient care, pointing to the importance of aggressive early nutrition.
 Effect of early nutrition on deaths due to severe traumatic brain injury. Journal of Neurosurgery. 109(1), 50 - 56.(2008).
Head injuries result in widespread brain tissue loss one year later
A study of traumatic brain injury (TBI) patients who span the full range of severity from mild to moderate and severe has revealed that the more severe the injury, the greater the loss of brain tissue one year after injury, particularly white matter. Researchers were surprised at the extent of tissue loss, which was widespread even in patients who had no obvious lesions, and was discernible even in the mild TBI group.
 The Toronto traumatic brain injury study: Injury severity and quantified MRI. Neurology. 70(10), 771 - 778.(2008).
Brain-injured war veterans show a faster decline in cognitive functioning as they age
A study of Vietnam war veterans who suffered brain injuries during the conflict has found that the men show a faster decline in their cognitive functioning as they grow older than veterans without such injuries. Greater intelligence and a higher level of education before the injury was sustained were associated with a smaller decline in cognitive functioning — perhaps because of a greater number of neural connections, enabling the brain to recover better from injury.
 Demographic, structural and genetic predictors of late cognitive decline after penetrating head injury. Brain: A Journal of Neurology. 131(Pt 2), 543 - 558.(2008).
Early lead exposure impedes later recovery from brain injury
We know that lead exposure in early years can affect the brain. We also know that it increases the risk of various disorders later in life. Now a rat study reveals that animals exposed to lead earlier in life were significantly less able to recover from an induced stroke than those not so exposed. The study only looked at a short time-frame, so it is not yet known if the lead-exposed animals would catch up in their recovery in a longer period of time. There was some recovery in the lead group, but then it leveled off. The control group continued to get better. The findings support the suggestion that lead poisoning impairs neural plasticity.
 Postnatal lead poisoning impairs behavioral recovery following brain damage. Neurotoxicology. 28(6), 1153 - 1157.(2007).
Imaging shows structural changes in mild traumatic brain injury
A study involving patients with all severities of traumatic brain injury has found that abnormalities in white matter existed across the spectrum, and that diffusion tensor imaging could identify structural changes even in patients with mild traumatic brain injury, who had minimal or no loss of consciousness, and even in those with no self-reported cognitive deficit. The imaging could also distinguish between axonal damage (tearing of the axons that allow one neuron to communicate with another) in white matter versus abnormalities in the myelin.
 White matter integrity and cognition in chronic traumatic brain injury: a diffusion tensor imaging study. Brain. 130(10), 2508 - 2519.(2007).
Stem cells improved memory in mice after brain injury
Brain damage in mice that significantly impaired memory was repaired through the introduction of neural stem cells. Interestingly, the stem cells did not primarily replace the dead neurons, but somehow supported the injured neurons by, it is thought, making beneficial proteins called neurotrophins. If so, it may be that a similar effect can be achieved by creating a drug that increases the release of neurotrophins.
 Neural Stem Cells Improve Memory in an Inducible Mouse Model of Neuronal Loss. J. Neurosci.. 27(44), 11925 - 11933.(2007).
Successful treatment for chronic TBI in rat study
A rat study has found that hyperbaric oxygen therapy (HBOT) improved spatial learning and memory in a model of chronic traumatic brain injury.
 Hyperbaric oxygen therapy improves spatial learning and memory in a rat model of chronic traumatic brain injury. Brain Research. 1174, 120 - 129.(2007).
Drug improves memory loss for traumatic brain injury patients
A study involving 157 men and women with traumatic brain injury found attention and verbal memory test scores significantly improved among those with moderate to severe memory impairment who took rivastigmine for 12 weeks. However, the drug was not effective for patients with less severe memory loss. Rivastigmine, a drug used to treat Alzheimer’s, is thought to enhance the function of acetylcholine, a neurotransmitter involved in memory and learning.
 Effects of rivastigmine on cognitive function in patients with traumatic brain injury. Neurology. 67(5), 748 - 755.(2006).
New research has demonstrated that adult mice produce multi-purpose, or progenitor, cells in the hippocampus, and indicates that the stem cells ultimately responsible for adult hippocampal neurogenesis actually reside outside the hippocampus, producing progenitor cells that migrate into the neurogenic zones and proliferate to produce new neurons and glia. The finding may help in the development of repair mechanisms for people suffering from dementia and acquired brain injury.
 The Adult Mouse Hippocampal Progenitor Is Neurogenic But Not a Stem Cell. J. Neurosci.. 25(47), 10815 - 10821.(2005).
Concussions increase chance of age-related cognitive impairment
A study involving retired National Football League players found that they had a 37% higher risk of Alzheimer's than other U.S. males of the same age. Some 60.8% of the retired players reported having sustained at least one concussion during their professional playing career, and 24% reported sustaining three or more concussions. Those with three or more concussions had a five-fold greater chance of having been diagnosed with mild cognitive impairment and a three-fold prevalence of reported significant memory problems compared to those players without a history of concussion. As the study was based on self-reported answers to the health questions, further studies are needed to confirm the findings, but it does seem likely that head injuries earlier in life increase the chance of developing dementia or mild cognitive impairment.
 Association between recurrent concussion and late-life cognitive impairment in retired professional football players. Neurosurgery. 57(4), 719-726; discussion 719-726 - 719-726; discussion 719-726.(2005).
Shift in brain's language-control site offers rehab hope
Language activity in right-handed people is initially localized in the left side of the brain, but a new study shows that this gradually becomes a function shared by both sides. From ages 5 to 25, language activity increases in the dominant hemisphere; from 25 to 67, the nondominant hemisphere increasingly shares the load. The discovery gives new hope for rehabilitation of brain function in adults after stroke or traumatic brain injuries.
 fMRI study of language lateralization in children and adults. Human Brain Mapping. 27(3), 202 - 212.(2006).
Post-concussion migraine may signal greater neurocognitive impairment
Another study suggesting sports’ concussions should be taken more seriously. The study found that young athletes who experienced migraine headache symptoms (even one week after concussion) were likely to have increased neurocognitive impairment. Headaches are reported in as many as 86% of such injuries; the researchers suggest that athletes should not be allowed to return to play before the headache resolves.
 Posttraumatic migraine characteristics in athletes following sports-related concussion. Journal of Neurosurgery. 102(5), 850 - 855.(2005).
Lead exposure may affect recovery from brain injury
Lead exposure at a young age can hurt the brain's development and cause learning and behavioral problems. Now it seems that it might also affect a child’s ability to recover from brain injury. A new study found young rats exposed to low levels of lead took significantly longer to recover from a brain injury than those animals that weren't lead-exposed, as well as recovering less well.
 Increasing Speed of Processing With Action Video Games. Current Directions in Psychological Science. 18(6), 321 - 326.(2009).
After serious head injury, survivors may still be able to learn without awareness
Severe closed-head injury (CHI), like that caused in a car accident, can impair the ability for purposeful learning. New research suggests however, that severe-CHI survivors may still be able to learn without awareness that they’re learning. In the first study of implicit learning in CHI using a perceptual task, participants were asked to identify the location of a target number -- 6 -- on a computer screen, as it moved in a seemingly random fashion around a matrix of numbers. The target’s location was actually determined by an underlying pattern of relationships between that location and the arrangement of other numbers in the display. Despite slower search rates, the CHI group’s improvement in locating the “6” was consistent with that of the control group. These findings suggest an alternative approach to remediation for such sufferers — for example, therapists could “teach” complex skills by breaking them down into sub-components that can be learned implicitly and/or made automatic. The findings also support the idea that different neural mechanisms might underlie explicit and implicit learning.
 Perceptually based implicit learning in severe closed-head injury patients. Neuropsychology. 16(1), 111 - 122.(2002).
Skill-specific exercises better for people who suffer from attention problems following stroke or brain injury
Treatment programs for people who suffer from attention problems following a stroke or other traumatic brain injuries often involve abstract cognitive exercises designed to directly restore impaired attention processes. But a review of 30 studies involving a total of 359 participants shows that an alternative and lesser-used therapy that teaches patients to relearn the tasks that affect their daily lives the most may be more effective. In this specific skills approach, people with brain damage learn to perform attention skills in a way that is different from non-brain-damaged people. In one study, for example, participants whose brain injuries affected their ability to drive a car used small electric cars in the lab to practice specific driving exercises, such as steering between pylons that were moved closer and closer together. Those that practiced specific exercises showed substantial improvement on a variety of driving related tasks compared to those who drove the car, but did not practice the exercises.
 Effectiveness of attention rehabilitation after an acquired brain injury: A meta-analysis.. Neuropsychology. 15(2), 199 - 210.(2001).