temporal lobe

one of the lobes of the cerebrum, situated below the frontal and parietal lobes, and above the hindbrain. The temporal lobe is primarily concerned with sensory experience - specifically, with hearing, and with the integration of information from multiple senses. Part of the temporal lobe also plays a role in memory processing. Patients with damaged temporal lobes appear to have impaired lexical retrieval of names of living things.

Exercise helps MCI

A pilot study involving 17 older adults with mild cognitive impairment and 18 controls (aged 60-88; average age 78) has found that a 12-week exercise program significantly improved performance on a semantic memory task, and also significantly improved brain efficiency, for both groups.

The program involved treadmill walking at a moderate intensity. The semantic memory tasks involved correctly recognizing names of celebrities well known to adults born in the 1930s and 40s (difficulty in remembering familiar names is one of the first tasks affected in Alzheimer’s), and recalling words presented in a list. Brain efficiency was demonstrated by a decrease in the activation intensity in the 11 brain regions involved in the memory task. The brain regions with improved efficiency corresponded to those involved in Alzheimer's disease, including the precuneus region, the temporal lobe, and the parahippocampal gyrus.

Participants also improved their cardiovascular fitness, by about 10%.

http://www.eurekalert.org/pub_releases/2013-07/uom-emb073013.php

Reference: 

Smith, J.C. et al. 2013. Semantic Memory Functional MRI and Cognitive Function After Exercise Intervention in Mild Cognitive Impairment. Journal of Alzheimer’s Disease, 37 (1), 197-215.

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Genes implicated in late-onset Alzheimer's disease

11 new genetic susceptibility factors for Alzheimer’s identified

The largest international study ever conducted on Alzheimer's disease (I-GAP) has identified 11 new genetic regions that increase the risk of late-onset Alzheimer’s, plus 13 other genes yet to be validated. Genetic data came from 74,076 patients and controls from 15 countries.

Eleven genes for Alzheimer's disease have previously been identified.

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Cognitive decline in old age related to poorer sleep

February, 2013

A new study confirms the role slow-wave sleep plays in consolidating memories, and reveals that one reason for older adults’ memory problems may be the quality of their sleep.

Recent research has suggested that sleep problems might be a risk factor in developing Alzheimer’s, and in mild cognitive impairment. A new study adds to this gathering evidence by connecting reduced slow-wave sleep in older adults to brain atrophy and poorer learning.

The study involved 18 healthy young adults (mostly in their 20s) and 15 healthy older adults (mostly in their 70s). Participants learned 120 word- nonsense word pairs and were tested for recognition before going to bed. Their brain activity was recorded while they slept. Brain activity was also measured in the morning, when they were tested again on the word pairs.

As has been found previously, older adults showed markedly less slow-wave activity (both over the whole brain and specifically in the prefrontal cortex) than the younger adults. Again, as in previous studies, the biggest difference between young and older adults in terms of gray matter volume was found in the medial prefrontal cortex (mPFC). Moreover, significant differences were also found in the insula and posterior cingulate cortex. These regions, like the mPFC, have also been associated with the generation of slow waves.

When mPFC volume was taken into account, age no longer significantly predicted the extent of the decline in slow-wave activity — in other words, the decline in slow-wave activity appears to be due to the brain atrophy in the medial prefrontal cortex. Atrophy in other regions of the brain (precuneus, hippocampus, temporal lobe) was not associated with the decline in slow-wave activity when age was considered.

Older adults did significantly worse on the delayed recognition test than young adults. Performance on the immediate test did not predict performance on the delayed test. Moreover, the highest performers on the immediate test among the older adults performed at the same level as the lowest young adult performers — nevertheless, these older adults did worse the following day.

Slow-wave activity during sleep was significantly associated with performance on the next day’s test. Moreover, when slow-wave activity was taken into account, neither age nor mPFC atrophy significantly predicted test performance.

In other words, age relates to shrinkage of the prefrontal cortex, this shrinkage relates to a decline in slow-wave activity during sleep, and this decline in slow-wave sleep relates to poorer cognitive performance.

The findings confirm the importance of slow-wave brainwaves for memory consolidation.

All of this suggests that poorer sleep quality contributes significantly to age-related cognitive decline, and that efforts should be made to improve quality of sleep rather than just assuming lighter, more disturbed sleep is ‘natural’ in old age!

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Alzheimer's protein may impair mental function even in healthy adults

March, 2012

The protein associated with Alzheimer's disease appears to impair cognitive function many years before symptoms manifest. Higher levels of this protein are more likely in carriers of the Alzheimer’s gene, and such carriers may be more affected by the protein’s presence.

Another study adds to the evidence that changes in the brain that may lead eventually to Alzheimer’s begin many years before Alzheimer’s is diagnosed. The findings also add to the evidence that what we regard as “normal” age-related cognitive decline is really one end of a continuum of which the other end is dementia.

In the study, brain scans were taken of 137 highly educated people aged 30-89 (participants in the Dallas Lifespan Brain Study). The amount of amyloid-beta (characteristic of Alzheimer’s) was found to increase with age, and around a fifth of those over 60 had significantly elevated levels of the protein. These higher amounts were linked with worse performance on tests of working memory, reasoning and processing speed.

More specifically, across the whole sample, amyloid-beta levels affected processing speed and fluid intelligence (in a dose-dependent relationship — that is, as levels increased, these functions became more impaired), but not working memory, episodic memory, or crystallized intelligence. Among the elevated-levels group, increased amyloid-beta was significantly associated with poorer performance for processing speed, working memory, and fluid intelligence, but not episodic memory or crystallized intelligence. Among the group without elevated levels of the protein, increasing amyloid-beta only affected fluid intelligence.

These task differences aren’t surprising: processing speed, working memory, and fluid intelligence are the domains that show the most decline in normal aging.

Those with the Alzheimer’s gene APOE4 were significantly more likely to have elevated levels of amyloid-beta. While 38% of the group with high levels of the protein had the risky gene variant, only 15% of those who didn’t have high levels carried the gene.

Note that, while the prevalence of carriers of the gene variant matched population estimates (24%), the proportion was higher among those in the younger age group — 33% of those under 60, compared to 19.5% of those aged 60 or older. It seems likely that many older carriers have already developed MCI or Alzheimer’s, and thus been ineligible for the study.

The average age of the participants was 64, and the average years of education 16.4.

Amyloid deposits varied as a function of age and region: the precuneus, temporal cortex, anterior cingulate and posterior cingulate showed the greatest increase with age, while the dorsolateral prefrontal cortex, orbitofrontal cortex, parietal and occipital cortices showed smaller increases with age. However, when only those aged 60+ were analyzed, the effect of age was no longer significant. This is consistent with previous research, and adds to evidence that age-related cognitive impairment, including Alzheimer’s, has its roots in damage occurring earlier in life.

In another study, brain scans of 408 participants in the Mayo Clinic Study of Aging also found that higher levels of amyloid-beta were associated with poorer cognitive performance — but that this interacted with APOE status. Specifically, carriers of the Alzheimer’s gene variant were significantly more affected by having higher levels of the protein.

This may explain the inconsistent findings of previous research concerning whether or not amyloid-beta has significant effects on cognition in normal adults.

As the researchers of the first study point out, what’s needed is information on the long-term course of these brain changes, and they are planning to follow these participants.

In the meantime, all in all, the findings do provide more strength to the argument that your lifestyle in mid-life (and perhaps even younger) may have long-term consequences for your brain in old age — particularly for those with a genetic susceptibility to Alzheimer’s.

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Obesity linked to better cognition in post-menopausal women

November, 2011

A new study suggests fat might help protect women from age-related cognitive decline.

Obesity has been linked to cognitive decline, but a new study involving 300 post-menopausal women has found that higher BMI was associated with higher cognitive scores.

Of the 300 women (average age 60), 158 were classified as obese (waist circumference of at least 88cm, or BMI of over 30). Cognitive performance was assessed in three tests: The Mini-Mental Statement Examination (MMSE), a clock-drawing test, and the Boston Abbreviated Test.

Both BMI and waist circumference were positively correlated with higher scores on both the MMSE and a composite cognitive score from all three tests. It’s suggested that the estrogen produced in a woman’s fat cells help protect cognitive function.

Interestingly, a previous report from the same researchers challenged the link found between metabolic syndrome and poorer cognitive function. This study, using data from a large Argentinean Cardiovascular Prevention Program, found no association between metabolic syndrome and cognitive decline — but the prevalence of metabolic syndrome and cognitive decline was higher in males than females. However, high inflammatory levels were associated with impairment of executive functions, and higher systolic blood pressure was associated with cognitive decline.

It seems clear that any connection between BMI and cognitive decline is a complex one. For example, two years ago I reported that, among older adults, higher BMI was associated with more brain atrophy (replicated below; for more recent articles relating obesity to cognitive impairment, click on the obesity link at the end of this report). Hypertension, inflammation, and diabetes have all been associated with greater risk of impairment and dementia. It seems likely that the connection between BMI and impairment is mediated through these and other factors. If your fat stores are not associated with such health risk factors, then the fat in itself is not likely to be harmful to your brain function — and may (if you’re a women) even help.

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Overweight and obese elderly have smaller brains

Analysis of brain scans from 94 people in their 70s who were still "cognitively normal" five years after the scan has revealed that people with higher body mass indexes had smaller brains on average, with the frontal and temporal lobes particularly affected (specifically, in the frontal lobes, anterior cingulate gyrus, hippocampus, and thalamus, in obese people, and in the basal ganglia and corona radiate of the overweight). The brains of the 51 overweight people were, on average, 6% smaller than those of the normal-weight participants, and those of the 14 obese people were 8% smaller. To put it in more comprehensible, and dramatic terms: "The brains of overweight people looked eight years older than the brains of those who were lean, and 16 years older in obese people." However, overall brain volume did not differ between overweight and obese persons. As yet unpublished research by the same researchers indicates that exercise protects these same brain regions: "The most strenuous kind of exercise can save about the same amount of brain tissue that is lost in the obese."

Reference: 

Zilberman, J.M., Del Sueldo, M., Cerezo, G., Castellino, S., Theiler, E. & Vicario, A. 2011. Association Between Menopause, Obesity, and Cognitive Impairment. Presented at the Physiology of Cardiovascular Disease: Gender Disparities conference, October 12, at the University of Mississippi in Jackson.

Vicario, A., Del Sueldo, M., Zilberman, J. & Cerezo, G.H. 2011. The association between metabolic syndrome, inflammation and cognitive decline. Presented at the European Society of Hypertension (ESH) 2011: 21st European Meeting on Hypertension, June 17 - 20, Milan, Italy.

[733] Thompson PM, Raji CA, Ho AJ, Parikshak NN, Becker JT, Lopez OL, Kuller LH, Hua X, Leow AD, Toga AW. Brain structure and obesity. Human Brain Mapping [Internet]. 2010 ;31(3):353 - 364. Available from: http://dx.doi.org/10.1002/hbm.20870

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Adolescent binge drinking can damage spatial working memory

August, 2011

This study finds that adolescent females are particularly vulnerable to the effects of binge drinking, and points to specific changes in brain activation patterns seen in binge drinkers.

Binge drinking occurs most frequently among young people, and there has been concern that consequences will be especially severe if the brain is still developing, as it is in adolescence. Because of the fact that it is only some parts of the brain — most crucially the prefrontal cortex and the hippocampus — that are still developing, it makes sense that only some functions will be affected.

I recently reported on a finding that binge drinking university students, performed more poorly on tests of verbal memory, but not on a test of visual memory. A new study looks at another function: spatial working memory. This task involves the hippocampus, and animal research has indicated that this region may be especially vulnerable to binge drinking. Spatial working memory is involved in such activities as driving, figural reasoning, sports, and navigation.

The study involved 95 adolescents (aged 16-19) from San Diego-area public schools: 40 binge drinking (27 males, 13 females) and 55 control (31 males, 24 females). Brain scans while performing a spatial working memory task revealed that there were significant gender differences in brain activation patterns for those who engaged in binge drinking. Specifically, in eight regions spanning the frontal cortex, anterior cingulate, temporal cortex, and cerebellum, female binge drinkers showed less activation than female controls, while male bingers exhibited greater activation than male controls. For female binge drinkers, less activation was associated with poorer sustained attention and working memory performances, while for male binge drinkers, greater activation was linked to better spatial performance.

The differences between male binge drinkers and controls were smaller than that seen in the female groups, suggesting that female teens may be particularly vulnerable. This is not the first study to find a gender difference in the brains’ response to excess alcohol. In this case it may have to do, at least partly, with differences in maturity — female brains mature earlier than males’.

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Long-term meditation fights age-related cognitive decline

August, 2011

Another study adds to the weight of evidence that meditating has cognitive benefits. The latest finding points to brain-wide improvements in connectivity.

Following on from research showing that long-term meditation is associated with gray matter increases across the brain, an imaging study involving 27 long-term meditators (average age 52) and 27 controls (matched by age and sex) has revealed pronounced differences in white-matter connectivity between their brains.

The differences reflect white-matter tracts in the meditators’ brains being more numerous, more dense, more myelinated, or more coherent in orientation (unfortunately the technology does not yet allow us to disentangle these) — thus, better able to quickly relay electrical signals.

While the differences were evident among major pathways throughout the brain, the greatest differences were seen within the temporal part of the superior longitudinal fasciculus (bundles of neurons connecting the front and the back of the cerebrum) in the left hemisphere; the corticospinal tract (a collection of axons that travel between the cerebral cortex of the brain and the spinal cord), and the uncinate fasciculus (connecting parts of the limbic system, such as the hippocampus and amygdala, with the frontal cortex) in both hemispheres.

These findings are consistent with the regions in which gray matter increases have been found. For example, the tSLF connects with the caudal area of the temporal lobe, the inferior temporal gyrus, and the superior temporal gyrus; the UNC connects the orbitofrontal cortex with the amygdala and hippocampal gyrus

It’s possible, of course, that those who are drawn to meditation, or who are likely to engage in it long term, have fundamentally different brains from other people. However, it is more likely (and more consistent with research showing the short-term effects of meditation) that the practice of meditation changes the brain.

The precise mechanism whereby meditation might have these effects can only be speculated. However, more broadly, we can say that meditation might induce physical changes in the brain, or it might be protecting against age-related reduction. Most likely of all, perhaps, both processes might be going on, perhaps in different regions or networks.

Regardless of the mechanism, the evidence that meditation has cognitive benefits is steadily accumulating.

The number of years the meditators had practiced ranged from 5 to 46. They reported a number of different meditation styles, including Shamatha, Vipassana and Zazen.

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Chronic jet lag has long-lasting effects on cognition

December, 2010

A hamster study indicates that chronic jet lag changes the brain in ways that cause long-lasting memory and learning problems.

Twice a week for four weeks, female hamsters were subjected to six-hour time shifts equivalent to a New York-to-Paris airplane flight. Cognitive tests taken during the last two weeks of jet lag and a month after recovery from it revealed difficulty learning simple tasks that control hamsters achieved easily. Furthermore, the jet-lagged hamsters had only half the number of new neurons in the hippocampus that the control hamsters had.

The findings support earlier research indicating that chronic jet lag impairs memory and learning and reduces the size of the temporal lobe, and points to the loss of brain tissue as being due to reduced neurogenesis in the hippocampus. Although further research is needed to clarify this, indications are that the problem is not so much fewer neurons being created, but fewer new cells maturing into working cells, or perhaps new cells dying prematurely.

Hamsters are excellent subjects for circadian rhythm research because their rhythms are so precise.

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Chemotherapy alters brain tissue in breast cancer patients

October, 2010

More evidence for the reality of ‘chemobrain’, showing physical changes in the brain.

Over the years I’ve reported on a number of studies investigating the effect of chemotherapy on the brain. A new study uses brain imaging, before and after treatment for breast cancer, to show that there is an anatomic basis for “chemobrain” complaints. The study, involving 17 breast cancer patients treated with chemotherapy after surgery, 12 women with breast cancer who did not undergo chemotherapy after surgery, and 18 women without breast cancer, found that gray matter density decreased in the frontal lobe, temporal lobe, cerebellum and right thalamus, shortly after chemotherapy.

The areas affected are consistent with memory and executive functions like multi-tasking and processing speed being the most typically affected functions. Post-surgery scans were carried out at one month, and at one year. Gray matter density in most women had improved by one year after chemotherapy ended.

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