The onset of ageing and age-related disorders may be delayed and even prevented completely, researchers from the Mayo Clinic wrote in the journal Nature. The scientists managed to delay and prevent the onset of muscle wasting, cataracts, and even wrinkles in an animal study carried out on mice by eliminating cells that build up with age – the scientists call them deadbeat cells or senescent cells.
The authors say this study is the first to show that deadbeat cells contribute to the ageing process. They added that they may have found a way of keeping people healthier as they get older.
Co-author James Kirkland, M.D., Ph.D., said:
“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. There is potential for a fundamental change in the way we provide treatment for chronic diseases in older people.”
Scientists found out about fifty years ago that cells only divide a certain number of times before the division stops altogether, at which point they reach cellular senescence – a state of limbo in which they are still alive, but do not continue multiplying. These deadbeat cells produce factors that harm the cells next to them, causing tissue inflammation.
Initially, these dysfunctional cells are regularly swept out by the body’s immune system. However, after some time these senescent cells start to accumulate because the immune system becomes less efficient at getting rid of them. This happens as we get older
Scientists have speculated that these cells cause age-related diseases, but nobody has been sure. Only between 10% to 15% of an elderly individuals cells are made up of senescent cells, making it harder to determine how important their role in the ageing process might be.
Senior author Jan van Deursen, Ph.D., said:
“Our discovery demonstrates that in our body cells are accumulating that cause these age-related disorders and discomforts. 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.”
Felipe Sierra, Ph.D., Director of the Division of Aging Biology, National Institute on Aging, National Institutes of Health, said:
“Through their novel methodology, the research team found that deletion of senescent cells in genetically engineered mice led to improvement in at least some aspects of the physiology of these animals. So, with the caveat that the study involved a mouse model displaying accelerated aging, this paper provides important insights on aging at the cellular level.”
Dr. van Deursen and team genetically engineered their laboratory mice so that their senescent cells carried caspase 8 – a molecule that is only turned on when the mice are given a drug that has no effect on normal cells. When they gave the mice the drug, caspase 8 became activated within the senescent cells, drilled holes in the membranes of those cells, effectively killing them.
They found that when the senescent cells were eliminated, the onset of age-related disorders, such as weakness, muscle loss, cataracts, etc., was delayed. Interestingly, when these cells were removed in the much older mice, the progression of age-related disorders that had been well underway was significantly slowed.
The scientists believe senescent cells play a role in the aging process. They also think that these cells secrete chemicals that contribute to disease and age-related tissue dysfunction.
Top Picture: Primary MEFs (mouse embryonic fibroblast cells) before senescence. They are spindle-shaped.
Bottom Picture: Example of cellular senescence. Cells become bigger, flatter shaped. They also express β-galactosidase (SABG, blue areas), a marker of cellular senescence.
The authors concluded in an Abstract in the journal:
“These data indicate that cellular senescence is causally implicated in generating age-related phenotypes and that removal of senescent cells can prevent or delay tissue dysfunction and extend healthspan.”
Written by Christian Nordqvist