20 September 2018


Scientists: clearing the brain of "zombie cells" slows down the development of dementia

RIA News

The removal of aged cells from the brain significantly slowed down its decrepitude and delayed the time of the appearance of the first symptoms of senile dementia in mice. This is written by biologists who published an article in the journal Nature (Bussian et al., Clearance of senescent glial cells prevents tau-dependent pathology and cognitive decline).

"It is clear that this approach cannot yet be applied in practice. Now we have started conducting experiments on animals after they develop Alzheimer's disease and other forms of dementia, and we are trying to understand what exactly changes in the work of microglial cells and astrocytes," said Darren Baker from the Mayo Clinic in In Rochester (in the press release Zombie cells found in brains of mice prior to cognitive loss – VM).

Embryo cells and embryonic stem cells are virtually immortal from the point of view of biology – they can live almost indefinitely in an adequate habitat, and divide an unlimited number of times. In contrast, adult body cells gradually lose their ability to divide after 40-50 division cycles, entering the aging phase, which presumably reduces the chances of developing cancer.

Why are they doing this? As scientists believe today, in this way cells protect themselves and the body as a whole from the development of cancer, stopping division at a time when the probability of mutations in their genome reaches a certain critical point. The decrepitude of the body, in turn, is a side effect of this process associated with the accumulation of "aged" cells in organs.

Two years ago, Baker and his colleagues discovered that removing such cells from the body using gene therapy or various medications significantly prolongs the life of experimental animals and reduces the likelihood of developing cancer and a number of other senile diseases.

This prompted them to think that removing similar cells from the brain could protect it from the accumulation of "protein debris" and the development of Alzheimer's, Parkinson's and other neurodegenerative diseases.

They tested this idea by slightly changing the technique they used during past experiments with mice. This time, they inserted a modified version of Cdkn2a, the "old age gene", not into all cells of the mice's body, but only in their nervous tissue, and used it to regularly "clean" the brain of elderly cells.

To do this, scientists fed them every two weeks with a special drug AP20187, which "turned on" an alternative version of Cdkn2a and forced the decrepit cells to destroy themselves without harming the rest of the body.

Subsequent observations showed that rodents undergoing such a "brainwashing" retained the ability to learn much longer and remembered new objects and events better than their relatives from the control group.

As a rule, mice of the breed with which Baker and his colleagues experimented fall into senile dementia at about 8 months of life. DNA modification and AP20187 reception delayed this date by several months, which is equivalent to several years of human life.

Interestingly, the deterioration of memory and mental acuity in old age was not due to the decrepitude of the brain neurons themselves, but their "servants" – microglia and astrocytes. These cells protect the brain from infections and supply it with energy and nutrients. Their "retirement", as the experiments of Baker's team have shown, contributes to the formation of protein "tangles" and other debris inside the brain.

A similar approach, as Baker notes, can be used to create drugs for Alzheimer's disease and other neurodegenerative diseases that develop in much the same way.

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