Distinguishing between driver and passenger mechanisms of aging
Nature genetics paper out today
Seems like it may be a highly relevant paper to us on this forum:
Understanding why we age is a long-standing question, and many mechanistic theories of aging have been proposed. Owing to limitations in studying the aging process, including a lack of adequate quantitative measurements, its mechanistic basis remains a subject of debate. Here, I explore theories of aging from the perspective of causal relationships. Many aging-related changes have been observed and touted as drivers of aging, including molecular changes in the genome, telomeres, mitochondria, epigenome and proteins and cellular changes affecting stem cells, the immune system and senescent cell buildup. Determining which changes are drivers and not passengers of aging remains a challenge, however, and I discuss how animal models and human genetic studies have been used empirically to infer causality.
Interesting read. Less directly applicable to us than I had hoped, but perhaps good to nudge the field a bit towards more mechanistic and causal understanding. Also a bit more pessimistic view on some of the progress than I think other leaders in the field would have.
An interesting quote….in support of animal models:
“ …animal models are not perfect representations of human biology. For example, laboratory mouse strains have long telomeres and high levels of telomerase, while humans have relatively short telomeres and, in most tissues, low levels of telomerase. Flies and worms, widely used models of aging, are mostly post-mitotic, while humans have both mitotic and post-mitotic tissues. As previously proposed, there are likely public and private mechanisms of aging, that is, mechanisms conserved across species and mechanisms of aging that are specific to individual species.”