Sedative senolytics
By destroying the "old age cells" in the brains of obese mice, scientists relieved them of anxiety (although they did not save them from obesity)
And along with the calmness, the normal growth of neurons returned
Polina Loseva, "The Attic"
Obesity leads to the accumulation of not only fat in the body, but also old non-working cells, which adversely affect neighbors, "aging" them as well. At the same time, the growth of adipose tissue correlates with changes in emotional state and the development of anxiety. An international group of scientists from the USA, England, Russia and Cyprus has established a direct link between these events. They selectively destroyed the senescent cells in the brains of obese mice, after which the anxiety of the animals disappeared, and the neurons began to grow better.
Like many other age-related diseases (such as osteoporosis, diabetes, muscle weakness and various inflammatory processes), obesity is accompanied by the appearance of senescent cells. These cells accumulate breakdowns, lose their original functions and harm their neighbors. In addition, old age at the cellular level turns out to be contagious: it is enough to transplant a small number of senescent cells to young ones in order to seriously undermine the health of the entire organism due to the fact that its cells will begin to "age" under the influence of aliens.
In this regard, one of the popular directions of modern anti–aging medicine are senolytics - drugs that selectively destroy senescent cells. This summer, the first clinical trials of senolytics on humans began, and in the meantime, scientists continue to understand how they act on the body.
A report on one such study has just been published in Cell Metabolism (Ogrodnik et al., Obesity-Induced Cellular Senescence Drives Anxiety and Impairs Neurogenesis). An international team of researchers, which includes employees of the Moscow Phys Tech, fattened mice to obesity in order to test the effectiveness of several methods of combating senescent cells on them. The number of senescent cells increased in the brains of the tested animals, fat droplets appeared in these cells, and the formation of new nerve cells and their processes stopped. In addition, compared to the control mice, the test mice behaved much more nervously: they clamped into corners, avoided open spaces and unfamiliar territories.
At the next stage, scientists tried to rid obese mice of senescent cells in their brains. There are two ways to deal with old cells – "from the inside" and "from the outside". In order for the old cells to kill themselves (the "inside out" method), scientists used genetically modified mice. Together with the p16 gene, which is considered a marker of senescent cells, they also activate the precursor gene of caspase-8, which can trigger apoptosis in the cell. "Outside" senescent cells can be destroyed with the help of senolytic drugs, such as dasatinib and quercetin, which, in fact, were fed to another part of obese mice.
Regardless of the way the cells were disposed of, the mice got better. Both methods did not cope, of course, with obesity directly, but under their influence the number of senescent cells and fat droplets in the brain sharply decreased, and along with this the anxiety of mice decreased and neurogenesis (growth of nerve cells and their processes) returned to the initial level.
And although this study shows this only in mice, people may already think that aging processes are involved even where they were not expected to be detected. This means that senolytics can find even wider application if they pass clinical trials.
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