Genetically modified centenarians

Roman Fishman, N+1 

American researchers have increased the lifespan of mice by up to 35% by simply cleansing their body of aged cells. The authors report on their work in the journal Nature (Baker et al., Naturally occurring p16INK4a-positive cells shorten healthy lifespan), as well as a press release from the Mayo Clinic Mayo Researchers Extend Lifespan in Mice by as Much as 35 Percent.

The team of Jan van Deursen used a line of transgenic mice INC-ATTAC, whose aged cells expressed not only their characteristic protein p16INK4a, but also two additional associated with it. This made such cells sensitive to the action of the synthetic agent AP20187, so that they were destroyed when the drug was injected into the body. Scientists have shown that mice subjected to this "cleansing of the body", after six months showed a markedly better state of health than the animals of the control group. They were more inquisitive and actively explored the space of the cell, they later developed tumor diseases, and life expectancy increased by 17 to 35%.

The idea that aged cells should be "destroyed before they destroy us" has been considered by scientists for quite a long time. Such cells with shortened telomeres do not just lose the ability to divide: the intensity of metabolism decreases in them, the accuracy of regulation of biochemical processes weakens, mutations accumulate faster. The immune system and apoptosis mechanisms help the body eliminate them, but they invariably accumulate with age. It has been shown that aged cells produce factors that damage neighboring tissues, secrete cytokines that lead to the development of chronic inflammation, provoke the development of tumors, type 2 diabetes mellitus and other age-related diseases.

In 2011 Van Dersen (Jan van Deursen) has already conducted similar experiments: by destroying some of the aged cells with the help of AP20187, scientists managed to increase the life span of animals by 20-25%. However, then the experiments were performed on INC-ATTAC mice obtained from a transgenic line mutated by the BubR1 gene. Such mice suffer from sarcopenia (muscular atrophy), cataracts and a host of other diseases, so their life turns out to be 4-5 times shorter than usual, so the conclusions of scientists could cause some doubts.

Despite this, even then the results stimulated pharmacologists to search for senolytic agents capable of selectively attacking aged cells without affecting others. In particular, in 2015, Van Dersen's colleague at the Mayo Clinic, James Kirkland, and co-authors found suitable effects in quercitin (a dietary supplement with a rather dubious background) and dasatinib (a patented antitumor drug). However, these works are still in the early stages of research.

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04.02.2015