. dSarm/Sarm1 is required for activation of an injury-induced axon death pathway. Science. 2012 Jul 27;337(6093):481-4. PubMed.

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  1. I believe that the discovery of dSarm/Sarm1 by Osterloh and colleagues as an endogenous regulator of Wallerian degeneration is a really exciting finding and a major step forward—this has really been what many of us in the field have been hoping for since Marc Freeman and others started studying Wallerian degeneration in flies a few years ago. This, finally, puts the notion of an endogenously regulated axon destruction program on firm ground. As is often the case for a newly implicated gene, we do not yet know how, or even where, Sarm1 acts to promote Wallerian degeneration—and from the previous pioneering efforts of Michael Coleman, Mark Freeman, and others on the original WLD-S fusion protein, we know this will not be a trivial task. But it will be a highly exciting one. This also means that it is currently difficult to gauge how important this—or related—axon destruction pathways might be in neurodegenerative diseases. Obviously, axons are a site of prime vulnerability in neurodegeneration. Still, as Wallerian degeneration is kicked off by an “initial” event, classically a transection, it is not straightforward to predict how preventing Wallerian degeneration will affect outcome in a given disease. A lot of this uncertainty stems from the fact that for most neurodegenerative conditions, we actually do not understand what the primary lesion to a neuron is. Indeed, it remains unclear why Wallerian degeneration is actually “there for,” and why it has been conserved. It will be exciting to see whether the newly identified dSarm/Sarm1 will be able to shed some light on such questions.

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