Why Aging Looks Tractable (Why Solve Aging: Part 5)

Why do we even think that it ought to be possible to develop drugs to delay or repair aging?  What makes this project look tractable?

  • Some animals are exceptionally long-lived; it looks like aging and lifespan are under evolutionary selection pressure. (If Nature can make some animals live much longer than their near relatives, perhaps we could as well.)

  • There are mutated strains of animals that live longer than the wild-type.  If genetic alterations can produce long life (and less age-related disease) then perhaps drugs could as well.

  • There are already many drugs that extend life in nematodes, fruit flies, and mice.  If they work on animals, some of those drugs might work to some extent on humans. In fact, many of the aging-related genetic pathways are conserved between species.  Genes associated with long life in humans can also extend life in lab animals.

  • There are many features and risk factors shared between the diseases of aging (things like metabolic syndrome and chronic inflammation, which are involved in cancer, heart disease, diabetes, Alzheimer’s, NAFLD, chronic kidney disease, and other age-related problems.)  While there may not be a single “root cause” of all aging, diseases of aging are often comorbid and share upstream types of dysfunction at the cellular level. This means that attacking common causes might be able to prevent all the major age-related diseases at once.

  • There haven’t been many resources devoted to aging as a field until recently; despite a large amount of low-hanging fruit, we’ve barely begun to explore the space of aging treatments. It’s also relatively recently that systematic, brute-force searches through genes and large phenotypic drug screens have become possible, which might allow us to systematically search for drugs that affect aging.

In subsequent posts, I’ll go into more detail on these individual factors.