Researchers at the Mayo Clinic have concluded that purging cells which accumulate with age could prevent or delay the onset of age-related disorders and disabilities.
The study – performed in mouse models – offers the first evidence that so-called “deadbeat” cells could contribute to aging.
“By attacking these cells and what they produce, one day we may be able to break the link between aging mechanisms and predisposition to diseases like heart disease, stroke, cancers and dementia,” explained James Kirkland, M.D., Ph.D., head of Mayo’s Robert and Arlene Kogod Center on Aging and the Noaber Foundation Professor of Aging Research.
“There is potential for a fundamental change in the way we provide treatment for chronic diseases in older people.”
Indeed, cells undergo a limited number of divisions before they stop dividing. At that point, cells reach a state of limbo – known as cellular senescence – where they neither die nor continue to multiply. Unfortunately, the “deadbeat” cells end up producing factors which damage adjacent cells and cause tissue inflammation.
This alternative cell fate is believed to be a mechanism to prevent runaway cell growth and the spread of cancer. Although the immune system sweeps out these dysfunctional cells on a regular basis, it becomes less effective at “keeping house” over time. As a result, senescent cells accumulate with age.
Whether and how these cells cause age-related diseases and dysfunction has been a major question in the field of aging. One reason the question has been so difficult to answer is that the numbers of senescent cells are quite limited and comprise at most only 10-15 percent of cells in an elderly individual.
“Our discovery demonstrates that in our body cells are accumulating that cause these age-related disorders and discomforts,” said Jan van Deursen, Ph.D., a Mayo Clinic molecular biologist and the Vita Valley Professor of Cellular Senescence.
“Therapeutic interventions to get rid of senescent cells or block their effects may represent an avenue to make us feel more vital, healthier, and allow us to stay independent for a much longer time.”
According to Deursen, the anti-aging effects of removing senescence cells was clearly illustrated when mice were genetically engineered so their senescent cells harbored a molecule called caspase 8 – which was only activated in the presence of a drug that has no effect on normal cells.
When the transgenic mice were exposed to this drug, caspase 8 was triggered, drilling holes in the cell membrane to specifically kill the senescent cells.
The researchers concluded that lifelong elimination of senescent cells delayed the onset of age-related disorders such as cataracts and muscle loss and weakness. As such, removing “deadbeat” cells later in life could slow the progression of already established age-related disorders.