Our Aging Cells

Aging and mortality are destinies we all share. But why would evolution produce such complex, sentient human beings, only to allow them to fail with age. Evolutionary biologists believe aging was programmed into our genetic code very early in evolution not for the benefit of the individual but for survival of the group.

Cells are the fundamental building blocks of all living organisms, providing the basic structure, extracting energy from food, following plans from genetic codes, and driving the processes required for growth, repair, and reproduction. Cells accumulate damage from DNA mutations, telomere shortening, oxidative stress, and other sources. Damage to DNA from any source that is not promptly repaired can trigger the cell's transition to a senescent state.

Although senescent cells lower cancer risk, these dysfunctional "zombie cells" accumulate with age. As dysfunctional non-dividing cells, they can no longer contribute to the specialized function of their tissues. They induce neighboring cells to become senescent and secrete toxic inflammatory signals that degrade surrounding tissues and drive age-related diseases. They stubbornly persist because, unlike most cells, they have evolved pathways that block apoptosis so they cannot commit suicide. These accumulated senescent cells are major contributors to the aging process.

As cells experience injuries throughout their lifetimes, the speed and effectiveness of their repair and regeneration systems strongly influence their survival. Thankfully, evolution has equipped us with powerful repair systems that routinely fix cellular damage often before it becomes irreversible. A growing body of evidence in animal studies suggests that repair systems are crucial in delaying aging, extending lifespan, and protecting against age-related diseases. The life of our cells is greatly dependent on the balance between cell damage and cell repair. A better understanding and more precise regulation of these cellular repair systems may offer powerful strategies for delaying aging and improving human longevity.

Investigators have identified fundamental biological processes, known as hallmarks of aging, that drive aging and age-related diseases. These pathways when accelerated can speed up aging and decrease lifespan and when mitigated can slow aging and extend lifespan. Cellular senescence, telomere attrition, stem cell exhaustion, and chronic inflammation are a few examples of these hallmarks.

Cellular senescence is considered one of the key "hallmarks of aging" because senescent cells accumulate in tissues with age and can disrupt normal function in all tissue types. Therapies that remove senescent cells (senolytics) or suppress their harmful secretions (senomorphics) are being investigated as treatments for both aging itself and chronic diseases of aging. Multiple animal studies have shown that senolytics can slow the features of aging, improve physical and cognitive function, and improve outcomes in several age-related disease models. This supports a new paradigm, the geroscience hypothesis, that treating hallmarks of aging up front may not only slow the aging process but may prevent or mitigate many diseases of aging at the same time

This paradigm contrasts with much of modern medicine, which has made major strides in diagnosing and treating chronic illness but typically kicks in only after symptoms appear, at which point significant damage may already have occurred. Although reactive care remains valuable, it often struggles to manage the complex web of chronic diseases of aging.

Because the new strategy will both delay the aging process and mitigate or prevent the chronic diseases of aging, it should be a very positive force at improving healthy lifespan (healthspan). Current lifespan in the U.SA. is about 79 years, while healthspan is about 68 years, meaning seniors will suffer with the chronic diseases of aging the last 11 years of their lives. Hopefully, as the new par