Slowing The Aging Process

Contributor
Graduate Division

Dr. Judith Campisi envisions a future where treatments would destroy cells that drive aging, thus lengthening our healthspan. Campisi delivered a seminar at UCSF on Oct. 24 describing her theory of senescent cell-driven aging.

Campisi, of the Buck Institute, has been a pioneer in the emerging field of gerontology, the study of aging. She believes senescent cells — those that have stopped dividing — are responsible for many of the changes we observe in our body as we age.

Campisi is a second generation Italian-American who spent her childhood in New York during the baby boomer years. In an interview with the American Society for Cell Biology, Campisi said she “received more than a Mendelian share of my Italian grandmother’s genes.”

That grandmother was a magician in the kitchen, a skill that lent itself nicely to Campisi’s choice upon entering university to study chemistry.

“The major difference between inspired experiments and inspired cooking is the success rate — that of cooking, alas, being much higher,” she said.

Following a handful of years in the blossoming pharmaceutical industry, Campisi completed a PhD in Biochemistry in New York before eventually establishing her own labs in Berkeley and the Buck Institute. During that time, her interests turned towards gerontology.

Campisi said she thinks that we have been thinking the wrong way about diseases that become more common with age, such as cancer, Alzheimer’s, and heart disease. These diseases are all extremely rare in young people.

“We think the reason very different diseases in very different tissues manifest on a similar trajectory over a lifespan is because there are a few basic processes driving all these diseases,” Campisi said during her recent seminar.

Her theory is that cellular senescence is one of these basic processes (inflammation is an example of another). We have known for decades of the existence of senescent cells, but little of what, if any, role they play in aging our bodies.

According to Campisi, as a byproduct of their development, senescent cells secrete a cocktail of molecules that can cause long term harm to the surrounding tissue, similar to chronic inflammation. As a result, cellular senescence may contribute to cancer progression and other aging associated diseases.

Then why do our cells deliberately become senescent? Isn’t it in their interest to stay viable for as long as possible?

Campisi thinks the answer lies in an apparent paradox: they may also be a form of defense against encroaching cancer.

Cancer involves uncontrolled cellular growth triggered by various damages that accumulate over life from such sources as UV light, carcinogens, and even physical wounds. Arresting a cell’s ability to multiply can stop cancer in its tracks, and we know that cellular senescence stops a cell from multiplying any further.

Cellular senescence, therefore, may have evolved to help maximize our survival chances during youth while indirectly wearing our body down as we age. To combat their effects on aging, we need to target and destroy these senescent cells.

“In theory if you can get senescent cells to die, you can retard cancer,” Campisi said.

To begin tackling this problem, she has helped found Unity Biotechnology, which aims to develop drugs specifically targeting these cells.

Campisi believes we will one day be able to optimize the beneficial effects of senescent cells and do away with the deleterious ones.

“We are well on our way to accomplishing that, but we still have a lot of work to do.”