A mouse model of retinal degeneration reveals a common mechanism for axonal degeneration and photoreceptor cell death and identifies SARM1 as a therapeutic candidate for retinopathies.

NMNAT1, a ubiquitously expressed metabolic enzyme linked to inherited blinding disease, is crucial for the proper differentiation of photoreceptor cells and subsequent survival of multiple cell types in the retina.

NMNAT is genetically required for glioma development and promotes glioma growth by allowing a higher tolerance to DNA damage and inhibiting DNA damage-p53-caspase-3 apoptosis signaling pathway by enhancing NAD⁺-dependent posttranslational modifications (PTMs) poly(ADP-ribosyl)ation (PARylation) and deacetylation of p53.

Mechanistic insight into the chaperone-like activity of NMNAT to phosphorylated Tau reveals a connection between NAD⁺metabolism and Tau homeostasis.

Genetic and biochemical analysis reveals that MAPK signaling promotes axon degeneration by modulating the turnover of axon-protective proteins.

Stable isotope labeling reveals that NAD crosses the inner membrane of mammalian mitochondria via an unknown transporter.

Axonal metabolic flux analysis demonstrates that expression of NMNAT1 blocks axonal degeneration in cultured mouse neurons not by altering NAD+ synthesis, but rather by inhibiting injury-induced, SARM1-dependent NAD+ consumption.

A function-based genetic screen using the Caenorhabditis elegans axotomy model identifies new regulators and an inhibitory role for NAD⁺ in axon regeneration, expanding the understanding of axon injury responses and regeneration.

Levels of the metabolite NMN, the precursor of NAD⁺, determine whether dSarm-mediated axon death signaling is activated and injury-induced axon degeneration executed in the fruit fly Drosophila.

TIR-1 regulates both repair and destruction on either side of an injury axon.