A paper in Nature touches on a most intriguing area of study: we know that telomeres tend to shorten and stem cells fail to replicate to repair tissue with increasing age, but what is the cart and what is the horse here? Do other modes of age-related cellular damage contribute to or result from these trends - to what degree and how? The science of aging is replete with questions of this ilk, as well as the strong sense that answers will come in the decade ahead. "[In some scenarios], the degree of telomere shortening can be correlated with disease duration, disease stage and severity as well as with response to disease-modifying treatment strategies. Whether increased telomere shortening represents a causal link between [hematopoietic stem cell (HSC)] turnover, replicative senescence and/or the induction of genetic instability in acquired HSC disorders remains to be shown. However, data from congenital disorders [suggest] that disturbed telomere maintenance may play a role for replicative exhaustion of the HSC pool in vivo."

View the Article Under Discussion: http://www.nature.com/leu/journal/vaop/ncurrent/abs/2404339a.html
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