Yo Sasaki

TL;DR: It is demonstrated that increased Nmnat activity is responsible for the axon-sparing activity of the Wlds protein and that SIRT1, a mammalian ortholog of Sir2, is the downstream effector of increased NMNat activity that leads to axonal protection.

TL;DR: It is shown that eNampt does not exert insulin-mimetic effects in vitro or in vivo but rather exhibits robust NAD biosynthetic activity, suggesting a vital framework for the regulation of glucose homeostasis.

TL;DR: Results strongly suggest that membrane ruffling and chemotaxis of microglia induced by ATP or ADP are mediated by Gi/o-coupled P2Y receptors.

TL;DR: NMN suppressed age-associated body weight gain, enhanced energy metabolism, promoted physical activity, improved insulin sensitivity and plasma lipid profile, and ameliorated eye function and other pathophysiologies and highlighted the preventive and therapeutic potential of NAD+ intermediates as effective anti-aging interventions in humans.

TL;DR: It is reported that SARM1 initiates a local destruction program involving rapid breakdown of nicotinamide adenine dinucleotide (NAD+) after injury and may explain the potent axon protection in Wallerian degeneration slow (Wlds) mutant mice.