Aging, longevity clues arise from gene study

Results of a recent study in mice may help guide therapies for Alzheimer’s disease and other aging-related diseases that target specific organs in humans, say researchers at the National Institutes of Health (NIH).

The investigators extended the average lifespan of a group of mice by about 20 percent by lowering the expression of a single gene called mTOR to the minimum level needed to survive. In humans, the increase would equate to 16 years, increasing the average lifespan from 79 to 95 years.

The genetically modified mice aged better overall, retained better memory and coordination as evidenced in maze and balance tests, and kept more muscle strength and posture when older. A loss of immune function, however, was suggested by an increased susceptibility to infections in old age, and the genetically modified mice also lost more bone volume than typical.

“While the high extension in lifespan is noteworthy, this study reinforces an important facet of aging: It is not uniform,” says lead researcher Toren Finkel, MD, PhD, at the NIH’s National Heart, Lung and Blood Institute (NHLBI). “Rather, similar to circadian rhythms, an animal might have several organ-specific aging clocks that generally work together to govern the aging of the whole organism.”

Additional studies in mice and humans are needed to identify exactly how aging in these different tissues is connected at the molecular level, the investigators say.

The study appeared in the Aug. 29 edition of Cell Reports. In addition to the NHLBI, the study was carried out by intramural researchers at the NIH’s National Cancer Institute, the National Institute of Diabetes and Digestive and Kidney Diseases and the National Institute on Aging.

Another recent mouse study, published in Nature, found that mice that inherit mutations of mitochondrial DNA from their mothers age more rapidly than mice without the DNA mutations.

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Lois Bowers

Lois A. Bowers was senior editor of I Advance Senior Care / Long-Term Living from 2013-2015.