Mental effort awakens anti-Alzheimer genes

With age, the risk of Alzheimer’s disease and other neuropsychiatric diseases, which are characterized by dementia, is increased – this is the term for persistent weakening of mental functions, from emotions to memory and learning ability. However, not all people are equally prone to dementia. Mental work is believed to be one of the factors that counteract cognitive decline. That is, a person whose life did not take place in a monotonous routine and who retained a love of intellectual leisure until old age is less likely to fall into senile dementia. This is confirmed not only in observations of people, but also in experiments with animals.

Mental effort and resistance to dementia must be linked by some mechanism. We often hear that a variety of stimuli that make the brain tense, contribute to the formation of new neural circuits: new synaptic contacts appear between neurons, and the pathways for signal transmission and processing become more diverse. A rich information life protects neurons from degradation. But the life of any cell depends on which genes are active in it and when exactly they are active.

Employees Massachusetts Institute of Technology write to Science Translational Medicinethat a variety of mental activities stimulate gene activity in the brain MEF2, and it is thanks to them that neurons resist extinction, and the brain as a whole resists dementia. Gene MEF2 encodes a protein that belongs to transcription factors, that is, it itself affects the activity of many other genes. First about MEF2 only knew that it helps to form the heart muscle during embryonic development. Then it turned out that he also plays a large role in the development of the nervous system and the functioning of neurons. MEF2 controls the genes encoding the proteins of ion channels, and as we know, the work of neurons is completely tied to ion channels: passing ions to the outer side of the membrane, then to the inner, ion channels change its electrical properties and thereby help launch an electrochemical impulse.

The researchers compared the activity MEF2 and those genes that depend on it, more than a thousand people. And those who more strongly resisted the disintegration of mental functions, the activity MEF2 and the genes under his jurisdiction was noticeably higher. Talking about work MEF2 within the same brain, then in “dementia-resistant” people MEF2 worked most strongly in groups of excitatory neurons in the prefrontal cortex. Excitatory neurons stimulate other neurons to be active (as opposed to inhibitory ones, which act as a sedative), and the prefrontal cortex is known to be involved in higher cognitive functions. It can be assumed, that MEF2 in excitatory neurons helps the prefrontal cortex to maintain a working shape.

The results obtained on human brain samples confirmed experiments with mice. The mice were either kept in an empty cage without toys, or in a cage with a squirrel wheel and toys, which were also changed every few days. As you might guess, in mice that lived in a cage with toys, MEF2 in the neurons of the brain was more active, and the mice themselves learned something new better. If MEF2 the animals were turned off, then even the varied environment in the cage did not help the mice to remain mindful and intelligent. And if mice were artificially stimulated in their youth MEF2then, with age, they had fewer accumulations of tau protein in the nervous tissue. Alzheimer’s disease and other neuropsychiatric disorders that lead to dementia are associated with the tau protein – accumulations of tau are toxic and cause neuronal death. That is, MEF2 suppressed the formation of dangerous protein deposits in the nervous tissue.

At the same time, what is important, the more active the gene was MEF2, the calmer the neurons behaved, and without MEF2 they became, on the contrary, hyperexcitable. It is known that in the early stages of neurodegenerative disorders, neurons start to work feverishly. Probably, MEF2 protects against various forms of dementia by preventing excitatory neurons from processing and overstraining the neural circuits that depend on them. (In general, over-excitability of neurons is a common problem not only for neurodegenerative diseases, but also for other neuropsychiatric disorders, such as schizophrenia and autism.)

Gen. MEF2 affects not only the genes of ion channels, and before coming up with a cure for dementia that would act on MEF2, you need to study how the changing activity MEF2 affects various cellular processes. At the same time, it would be curious to find out exactly how diverse life is transmitted to molecular genetic processes, or, in other words, what physiological, biochemical, molecular signals connect mental efforts and the piece of DNA in which the gene is encoded MEF2.

Source: Автономная некоммерческая организация "Редакция журнала «Наука и жизнь»" by

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