Study Finds Senescent Cells Accelerate the Aging Process

“People used to see aging as a rusting nail — there’s nothing you can do about it. But we now know that there are processes that are driving aging, and that those processes can be meddled with.” –Dr. Campisi (Buck Institute for Research on Aging).

When a cell looses the ability to divide, usually after approximately 50 cell divisions, it undergoes what is known as cell senescence. A combination of environmental and genetic factors may contribute to cell senescence, including DNA damage  and shortened telomeres. When a cell dies, it might benefit the entire organism as a whole, but when cell senescence occurs as part of the aging process, the organism looses it potential to respond to stress, and becomes more prone to age-related illnesses, such as heart disease and cancer. The Integrative Genomics of Aging Group states that organismal aging is a process defined as “a progressive deterioration of physiological function, an intrinsic age-related process of loss of viability and increased vulnerability.”

But there are differences in lifespan across species, and within humans, because different people, and other animals, age at different rates. Over several years of cell division, telomeres have been shown to shorten, prompting the cell to “commit suicide” or stop dividing and enter a semi-retired state called replicative senescence. “As more and more cells die,” says a 2011 Science Magazine article, “the skin, the lining of the intestines, and other tissues can gradually lose the capacity to replenish themselves.”

In a Nov. 2 article published in the New York Times, researchers say that cleansing the body of senescent cells, which spur the aging of tissues, may postpone many of the diseases associated with aging.

This research raises the possibility that therapies that cleanse the body of senescent cells may ameliorate or even reverse some of the damaging effects of aging. But many scientists say that more tests are needed before specific therapies or drugs can be developed to increase people’s lifespan or health span.

Senescent cells can stick to aging tissues, including arthritic joints, cataracts, and even the plaque that lines the arteries of older individuals, prompting the immune system to act and causing mild inflammation. It has also been found that senescent cells accelerate aging in the tissues in which they accumulate.

To test for the effects on the aging process in organisms without these cells, Darren J. Baker and Jan M. van Deursen–researchers at the Mayo Clinic in Rochester, Minn.– genetically engineered a strain of mouse in which all senescent cells were programmed to self-destruct.

The results? Mice without a deleterious accumulation of senescent cells showed significantly better health than their unaltered counterparts. The group without these cells did not develop cataracts, maintained muscle mass usually wasted with age, and were able to sustain longer exercise periods on a mouse treadmill.  Additionally, the mice without harmful senescent cells kept fat in the skin that is typically loss with age. In humans, this process causes skin wrinkling.

According to many aging experts, including Dr. Normal E. Sharpless of the University of North Carolina, this is a fundamental advance in the field of aging, largely because it’s the first study of its kind, and also because the discovery that senescent cells cause tissue degradation opens a new terrain for researchers and scientists to explore.

Judith Campisi, from the Buck Institute for Research on Aging, called the study a “breakthrough.”

Although there are many questions about aging that this study brings up–such as when it would be most beneficial in an organism’s lifetime to remove senescent cells, and whether preexisting tissue damage due to the aging process could be reversed by senescent cell therapy—a main takeaway point, says Dr. Campisi, is that the purpose of age research is not to make people immortal, as many sensationalized claims suggest, but rather to improve health span, which is the ratio of people’s overall lifespan to the number of those years they lived in good health.