Cellular senescence refers to the state at which a cell in the body can no longer divide. As we age, more and more cells become senescent.
Research has revealed that the presence of senescent cells is worse than one might think. These cells assume a special secretory form (SASP) in which they release various chemical signals that harm the health of nearby cells. In a domino effect they then damage their neighbors further accelerating the aging process.
A breakthrough study earlier this year showed that using specialized genetic methods to remove senescent cells throughout the lifespan of rats reduced signs of aging in the animals.
The current state of the science review article, referenced below, is written by two of the scientists who perform that study, DJ Baker and JM van Deursen.
In the paper they describe how senescent cells lead to aging in many tissues in the body. They further point out that aging of tissue is the reason for the development of diseases.
“Therapeutic intervention in normal aging may prevent comorbidity and delay mortality in the elderly,” they write. “In this way, targeting of senescent cells during the course of normal aging would be a preventative strategy rather than a treatment.”
This statement of course is the crux of the issue and a key concept to allow for mass acceptance of life extension medicine.
The different tissue systems in which the authors point out the damaging effect of senescent cells and potential for prevention include: cancer, type II diabetes, lung disease (COPD), arthritis, Parkinson’s disease, Alzheimer’s diease, and eye diseases including cataracts glaucoma, and macular degeneration. Even skin appearance could be improved.
It is also pointed out that senescent stem cells may poison stem cell niches reducing the ability to regenerate and rejuvenate tissue so that removing them there could have diffuse age reducing benefit.
Of course the big question is how senescent cells could be regularly removed from all over and within the human body other than embedding programmable genes before birth like was done in lab rats.
The answers remain vague but the authors offer an idea, and some hope:
“If a common signature is identified for senescent cells in vivo, strategies to alleviate these effects with compounds or drugs, whether by dampening the SASP profile or by completely removing the senescent cells, can begin to be elucidated.”