frontal lobe

the frontal lobes (left and right) are situated at the "front" of the cortex, i.e. behind the forehead. They are the largest of the lobes in the cerebrum, and may be thought of as the "highest" part of our brain. The frontal lobes are critical for those faculties that humans regard as special to our species - reasoning, planning, attention, some aspects of language. Women have up to 15% more brain cell density in the frontal lobe, but with age, appear to shed cells more rapidly from this area than men. By old age, the density is similar for both sexes. The effect of this on performance is unknown.

Diabetes and tau tangles linked independently of Alzheimer's

  • Type 2 diabetes is known to increase the risk of Alzheimer's disease.
  • In a reasonably large study, diabetes was found to be linked with higher levels of tau protein, regardless of the presence of dementia.
  • Diabetes was also linked with greater brain shrinkage.
  • The finding adds to evidence that diabetes increases the risk of cognitive impairment in old age.

A study involving older adults has found that diabetes was associated with higher levels of tau protein and greater brain atrophy.

The study involved 816 older adults (average age 74), of whom 397 had mild cognitive impairment, 191 had Alzheimer's disease, and 228 people had no cognitive problems. Fifteen percent (124) had diabetes.

Those with diabetes had greater levels of tau protein in the spinal and brain fluid regardless of cognitive status. Tau tangles are characteristic of Alzheimer's.

Those with diabetes also had cortical tissue that was an average of 0.03 millimeter less than those who didn't have diabetes, regardless of their cognitive status. This greater brain atrophy in the frontal and parietal cortices may be partly related to the increase in tau protein.

There was no link between diabetes and amyloid-beta, the other main pathological characteristic of Alzheimer's.

Previous research has indicated that people with type 2 diabetes have double the risk of developing dementia. Previous research has also found that those who had been diabetic for longer had a greater degree of brain atrophy

The findings support the idea that type 2 diabetes may have a negative effect on cognition independent of dementia, and that this effect may be driven by an increase in tau phosphorylation.

http://www.eurekalert.org/pub_releases/2015-09/aaon-dab082715.php

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Movie study confirms older people are more distractible

Idiosyncratic brain activity among older people watching a thriller-type movie adds to evidence that:

  • age may affect the ability to perceive and remember the order of events (explaining why older adults may find it harder to follow complex plots)
  • age affects the ability to focus attention and not be distracted
  • age affects the brain's connectivity — how well connected regions work together.

A study involving 218 participants aged 18-88 has looked at the effects of age on the brain activity of participants viewing an edited version of a 1961 Hitchcock TV episode (given that participants viewed the movie while in a MRI machine, the 25 minute episode was condensed to 8 minutes).

While many studies have looked at how age changes brain function, the stimuli used have typically been quite simple. This thriller-type story provides more complex and naturalistic stimuli.

Younger adults' brains responded to the TV program in a very uniform way, while older adults showed much more idiosyncratic responses. The TV program (“Bang! You're dead”) has previously been shown to induce widespread synchronization of brain responses (such movies are, after all, designed to focus attention on specific people and objects; following along with the director is, in a manner of speaking, how we follow the plot). The synchronization seen here among younger adults may reflect the optimal response, attention focused on the most relevant stimulus. (There is much less synchronization when the stimuli are more everyday.)

The increasing asynchronization with age seen here has previously been linked to poorer comprehension and memory. In this study, there was a correlation between synchronization and measures of attentional control, such as fluid intelligence and reaction time variability. There was no correlation between synchronization and crystallized intelligence.

The greatest differences were seen in the brain regions controlling attention (the superior frontal lobe and the intraparietal sulcus) and language processing (the bilateral middle temporal gyrus and left inferior frontal gyrus).

The researchers accordingly suggested that the reason for the variability in brain patterns seen in older adults lies in their poorer attentional control — specifically, their top-down control (ability to focus) rather than bottom-up attentional capture. Attentional capture has previously been shown to be well preserved in old age.

Of course, it's not necessarily bad that a watcher doesn't rigidly follow the director's manipulation! The older adults may be showing more informed and cunning observation than the younger adults. However, previous studies have found that older adults watching a movie tend to vary more in where they draw an event boundary; those showing most variability in this regard were the least able to remember the sequence of events.

The current findings therefore support the idea that older adults may have increasing difficulty in understanding events — somthing which helps explain why some old people have increasing trouble following complex plots.

The findings also add to growing evidence that age affects functional connectivity (how well the brain works together).

It should be noted, however, that it is possible that there could also be cohort effects going on — that is, effects of education and life experience.

http://www.eurekalert.org/pub_releases/2015-08/uoc-ymt081415.php

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Crucial factors in the evolution of the human brain

September, 2012

Two recent studies comparing gene expression in the brains of human and other animals reveal a key protein for brain size and others for connectivity and regulation.

Genetic comparisons have pinpointed a specific protein as crucial for brain size, both between and within species. Another shows how genetic regulation in the frontal lobes distinguishes the human brain from that of closely related species, and points to two genes in particular as critical.

The protein determining brain size

Comparison of genome sequences from humans and other animals has revealed what may be a crucial protein in the development of the human brain. The analysis found that humans have more than 270 copies of a protein called DUF1220 — more than any other animal studied — and that the number of copies in a species seems to match how close they are to us. Chimpanzees, for example, have 125, and gorillas 99, while marmosets have only 30, and mice just one.

Moreover, comparison of humans with microcephaly and macrocephaly reveals that those with microcephaly (“small brain”) have lower numbers of this protein than normal for humans, and those with macrocephaly (“large brain”) have higher numbers. Copy numbers of the protein were also correlated with gray matter volume in humans without these brain disorders.

In other words, evidence from three lines of inquiry converge on DUF1220 copy number being associated with brain size.

Differences in gene expression and connectivity

But the development of the human brain is not only about size. The human brain is more complex, more connected, than the brains of most other animals. Another genetic analysis has been comparing gene activity in humans, chimpanzees and rhesus macaques, using post-mortem brain tissue of three regions in particular – the frontal cortex, hippocampus and striatum.

Gene expression in the frontal lobe of humans showed a striking increase in molecular complexity, with much more elaborate regulation and connection. The biggest differences occurred in the expression of human genes involved in plasticity.

One gene in particular stood out as behaving differently in the human brain. This gene — called CLOCK, for obvious reasons — is thought to be the master regulator of our body’s clocks. The finding suggests it has influence beyond this role. Interestingly, this gene is often disrupted in mood disorders such as depression and bipolar syndrome.

A second important distinction was how many more connections there were in human brains among networks that included the language genes FOXP1 and FOXP2.

In comparison to all this, gene expression in the caudate nucleus was very similar across all three species.

The findings point to the role of learning (the genes involved in plasticity) and language in driving human brain evolution. They also highlight the need to find out more about the CLOCK gene.

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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, P. M., Raji C. A., Ho A. J., Parikshak N. N., Becker J. T., Lopez O. L., et al.
(2010).  Brain structure and obesity.
Human Brain Mapping. 31(3), 353 - 364.

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Running faster changes brain rhythms associated with learning

September, 2011

A mouse study finds that gamma waves in the hippocampus, critically involved in learning, grow stronger as mice run faster.

I’ve always felt that better thinking was associated with my brain working ‘in a higher gear’ — literally working at a faster rhythm. So I was particularly intrigued by the findings of a recent mouse study that found that brainwaves associated with learning became stronger as the mice ran faster.

In the study, 12 male mice were implanted with microelectrodes that monitored gamma waves in the hippocampus, then trained to run back and forth on a linear track for a food reward. Gamma waves are thought to help synchronize neural activity in various cognitive functions, including attention, learning, temporal binding, and awareness.

We know that the hippocampus has specialized ‘place cells’ that record where we are and help us navigate. But to navigate the world, to create a map of where things are, we need to also know how fast we are moving. Having the same cells encode both speed and position could be problematic, so researchers set out to find how speed was being encoded. To their surprise and excitement, they found that the strength of the gamma rhythm grew substantially as the mice ran faster.

The results also confirmed recent claims that the gamma rhythm, which oscillates between 30 and 120 times a second, can be divided into slow and fast signals (20-45 Hz vs 45-120 Hz for mice, consistent with the 30-55 Hz vs 45-120 Hz bands found in rats) that originate from separate parts of the brain. The slow gamma waves in the CA1 region of the hippocampus were synchronized with slow gamma waves in CA3, while the fast gamma in CA1 were synchronized with fast gamma waves in the entorhinal cortex.

The two signals became increasingly separated with increasing speed, because the two bands were differentially affected by speed. While the slow waves increased linearly, the fast waves increased logarithmically. This differential effect could have to do with mechanisms in the source regions (CA3 and the medial entorhinal cortex, respectively), or to mechanisms in the different regions in CA1 where the inputs terminate (the waves coming from CA3 and the entorhinal cortex enter CA1 in different places).

In the hippocampus, gamma waves are known to interact with theta waves. Further analysis of the data revealed that the effects of speed on gamma rhythm only occurred within a narrow range of theta phases — but this ‘preferred’ theta phase also changed with running speed, more so for the slow gamma waves than the fast gamma waves (which is not inconsistent with the fact that slow gamma waves are more affected by running speed than fast gamma waves). Thus, while slow and fast gamma rhythms preferred similar phases of theta at low speeds, the two rhythms became increasingly phase-separated with increasing running speed.

What’s all this mean? Previous research has shown that if inputs from CA3 and the entorhinal cortex enter CA1 at the same time, the kind of long-term changes at the synapses that bring about learning are stronger and more likely in CA1. So at low speeds, synchronous inputs from CA3 and the entorhinal cortex at similar theta phases make them more effective at activating CA1 and inducing learning. But the faster you move, the more quickly you need to process information. The stronger gamma waves may help you do that. Moreover, the theta phase separation of slow and fast gamma that increases with running speed means that activity in CA3 (slow gamma source) increasingly anticipates activity in the medial entorhinal cortex (fast gamma source).

What does this mean at the practical level? Well at this point it can only be speculation that moving / exercising can affect learning and attention, but I personally am taking this on board. Most of us think better when we walk. This suggests that if you’re having trouble focusing and don’t have time for that, maybe walking down the hall or even jogging on the spot will help bring your brain cells into order!

Pushing speculation even further, I note that meditation by expert meditators has been associated with changes in gamma and theta rhythms. And in an intriguing comparison of the effect of spoken versus sung presentation on learning and remembering word lists, the group that sang showed greater coherence in both gamma and theta rhythms (in the frontal lobes, admittedly, but they weren’t looking elsewhere).

So, while we’re a long way from pinning any of this down, it may be that all of these — movement, meditation, music — can be useful in synchronizing your brain rhythms in a way that helps attention and learning. This exciting discovery will hopefully be the start of an exploration of these possibilities.

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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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Sleep and memory - round-up of recent reports

July, 2011

A round-up of recent reports relating to the role of sleep in consolidating memory.

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.

 

Reference: 

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.

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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

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The importance of the cerebellum for intelligence and age-related cognitive decline

March, 2011
  • A new study of older adults indicates atrophy of the cerebellum is an important factor in cognitive decline for men, but not women.

Shrinking of the frontal lobe has been associated with age-related cognitive decline for some time. But other brain regions support the work of the frontal lobe. One in particular is the cerebellum. A study involving 228 participants in the Aberdeen Longitudinal Study of Cognitive Ageing (mean age 68.7) has revealed that there is a significant relationship between grey matter volume in the cerebellum and general intelligence in men, but not women.

Additionally, a number of other brain regions showed an association between gray matter and intelligence, in particular Brodmann Area 47, the anterior cingulate, and the superior temporal gyrus. Atrophy in the anterior cingulate has been implicated as an early marker of Alzheimer’s, as has the superior temporal gyrus.

The gender difference was not completely unexpected — previous research has indicated that the cerebellum shrinks proportionally more with age in men than women. More surprising was the fact that there was no significant association between white memory volume and general intelligence. This contrasts with the finding of a study involving older adults aged 79-80. It is speculated that this association may not develop until greater brain atrophy has occurred.

It is also interesting that the study found no significant relationship between frontal lobe volume and general intelligence — although the effect of cerebellar volume is assumed to occur via its role in supporting the frontal lobe.

The cerebellum is thought to play a vital role in three relevant areas: speed of information processing; variability of information processing; development of automaticity through practice.

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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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Adolescents with type 2 diabetes have diminished cognitive performance and brain abnormalities

September, 2010

Another study adds to growing evidence that diabetes, or poor glycaemic control, has serious implications for brain function.

A small study comparing 18 obese adolescents with type 2 diabetes and equally obese adolescents without diabetes or pre-diabetes has found that those with diabetes had significantly impaired cognitive performance, as well as clear abnormalities in the integrity of their white matter (specifically, reduced white matter volume, especially in the frontal lobe, as well as impaired integrity in both white and grey matter). Similar abnormalities have previously been found in adults with type 2 diabetes, but the subjects were elderly and, after many years of diabetes, generally had significant vascular disease. One study involving middle-aged diabetics found a reduction in the volume of the hippocampus, which was directly associated with poor glycaemic control.

It remains to be seen whether such changes can be reversed by exercise and diet interventions. While those with diabetes performed worse in all cognitive tasks tested, the differences were only significant for intellectual functioning, verbal memory and psychomotor efficiency.

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