Turning Back the Clock: The Quest to Reverse Aging at the Cellular Level
The Loss of Cellular Identity Drives Aging
According to Harvard geneticist David Sinclair, aging occurs due to a loss of information within our cells over time. This erosion of fidelity causes cells to lose their identity and function. He relates this to pioneering information theorist Claude Shannon’s concept of information loss occurring during transmission of signals.
The regulators of gene expression called sirtuins seem to play an integral role in this process. As cells encounter stresses and need to activate repair mechanisms, sirtuins relocate from their regular duty of silencing genes. Over decades of life, this back and forth leads cells to gradually “forget” which genes should be on or off.
Methylation Patterns Form an “Aging Clock”
Particular patterns of DNA methylation, which help control gene expression through gene silencing, correlate strongly with chronological age. They effectively form an epigenetic aging clock ticking away in every cell.
This clock starts running from the beginning of embryonic development through to adulthood and old age. The pace of methylation accelerates with environmental factors like smoking, while lifestyle interventions like exercise may slow it slightly.
Reprogramming Cells Can Restore a More Youthful State
Sinclair’s lab delivered modified stem cell genes called Yamanaka factors via engineered viruses to retinal cells in aged mice. This induced partial cellular reprogramming, altering gene expression and restoring a more youthful methylation pattern.
In mice with crushed optic nerves, this reprogramming enabled nerve regeneration and restoration of vision. It reactivated youthful gene expression programs that are usually lost with aging.
Cells Retain an Imprint of Their Original Youthful State
The precise tuning of hundreds of genes back to near-original youthful levels suggests cells harbor an intrinsic backup mechanism to access the original gene expression pattern.
Like Claude Shannon’s concept of error checking information channels, cells seem to retain an ‘observer’ copy of the youthful epigenetic program to restore from. This program gets obscured but remains largely intact over a lifetime, unless it gets accessed by reprogramming.
The potential now exists to develop interventions leveraging this backup mechanism to partially turn back the aging clock within cells. However, reprogramming too intensely can also be damaging and needs to walk a fine line.
