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.

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

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

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.

Reproductive fluids help the correct establishment of some epigenetic marks and gene expression in preimplantation pig embryos.

Neurotrophin deprivation leads to rapid caspase-independent disassembly of the actin-spectrin-based membrane skeleton and spectrin-dependent retrograde signaling in axon degeneration.

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

New technology for manipulating genes in Drosophila facilitates gene tagging and precise modification of virtually any gene.

Stimulation of the rate-limiting enzyme in the NAD salvage pathway protected against neurotoxicity and subsequent peripheral neuropathy associated with the widely utilized anticancer drug, paclitaxel.

Anti-inflammatory effects of resveratrol are mediated by the estrogen receptor to coordinate a complex array of transcriptional coregulators, suggesting that estrogenic effects must be considered in the complex polypharmacology of resveratrol.