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Brain Regions

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Two recent conference presentations add to the evidence for the benefits of ‘brain training’, and of mental stimulation, for holding back age-related cognitive decline.

My recent reports on brain training for older adults (see, e.g., Review of working memory training programs finds no broader benefit;

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.

In another example of how expertise in a specific area changes the brain, brain scans of piano tuners show which areas grow, and which shrink, with experience — and starting age.

I’ve reported before on how London taxi drivers increase the size of their posterior hippocampus by acquiring and practicing ‘the Knowledge’ (but perhaps at the expense of other functions).

Emotionally arousing images that are remembered more vividly were seen more vividly. This may be because the amygdala focuses visual attention rather than more cognitive attention on the image.

Two new studies provide support for the judicious use of sleep learning — as a means of reactivating learning that occurred during the day.

Back when I was young, sleep learning was a popular idea. The idea was that a tape would play while you were asleep, and learning would seep into your brain effortlessly. It was particularly advocated for language learning.

  • For those with the Alzheimer’s gene, higher blood pressure, even though within the normal range, is linked to greater brain shrinkage and reduced cognitive ability.

I’ve reported before on the evidence suggesting that carriers of the ‘Alzheimer’s gene’, APOE4, tend to have smaller brain volumes and perform worse on cognitive tests, despite being cognitively ‘normal’.

  • People with a strong genetic risk of early-onset Alzheimer’s have revealed a progression of brain changes that begin 25 years before symptoms are evident.

A study involving those with a strong genetic risk of developing Alzheimer’s has found that the first signs of the disease can be detected 25 years before symptoms are evident.

Further evidence from mice studies that the Easter Island drug improves cognition, in young mice as well as old.

I have reported previously on research suggesting that rapamycin, a bacterial product first isolated from soil on Easter Island and used to help transplant patients prevent organ rejection, might improve learning and memory.

A small study supports the view that excess activity in the hippocampus seen in aMCI is not compensatory but a sign of dysfunction, and shows that an epileptic drug reduces activity and improves memory.

Interpreting brain activity is a very tricky business. Even the most basic difference can be interpreted in two ways — i.e., what does it mean if a region is more active in one group of people compared to another?

A round-up of genetic news.

  • Several genes are linked to smaller brain size and faster brain atrophy in middle- & old age.
  • The main Alzheimer's gene is implicated in leaky blood vessels, and shown to interact with brain size, white matter lesions, and dementia risk.
  • Some evidence suggests early-onset Alzheimer's is not so dissimilar to late-onset Alzheimer's.

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).

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