The molecular basis of aging
Is aging an inevitable wearing-down, or a program we could one day slow or reverse?
What makes this fascinating
The hallmarks of aging — Researchers catalog a dozen shared processes — telomere loss, senescent cells, epigenetic drift — but not which are causes and which are symptoms.
Program or wear-and-tear? — Is aging an evolved program or just accumulated damage? The answer decides whether it can ever be slowed or reversed.
Already reversible in the lab — Cellular reprogramming and senolytic drugs have extended healthy lifespan in mice; translating that to humans is the open frontier.
Frequently asked questions
- What causes aging?
- Aging stems from accumulating molecular and cellular damage — DNA damage, telomere shortening, protein misfolding, cellular senescence, and mitochondrial decline. Whether these are root causes or downstream symptoms of a deeper program is unresolved.
- Can aging be slowed or reversed?
- In animals, interventions like caloric restriction, senolytics, and partial cellular reprogramming have extended lifespan or reversed some markers. Whether human aging can be substantially slowed or reversed is still an open question.
- Is aging a disease?
- That is debated. Some researchers argue aging should be treated as a disease because it is the primary risk factor for cancer, heart disease, and dementia; others view it as a natural process.
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