Among its various biological functions, NAD metabolism regulates axon degeneration, which is an early and often causative event in a variety of neurodegenerative diseases including Huntington’s disease (HD) and Alzheimer’s disease (AD).Our research group previously found that reducing the levels of the NAD precursor nicotinamide mononucleotide (NMN) pharmacologically with the NMN synthesizing enzyme nicotinamide phosphoribosyl transferase (NAMPT) inhibitor FK866 or genetically by expressing the bacterial enzyme NMN deamidase in mammalian neurons remarkably reduces axon degeneration after acute injury. Here, we asked whether FK866 could also improve axonal pathology and behavioral symptoms in in vitro and in vivo models of HD and AD, and compared its effect to that of memantine, an N methyl D aspartate receptor (NMDAR) antagonist with a well defined neuroprotective action.An inducible PC12 cell line expressing wild type (Q21 PC12 cells) and HD associated mutant Huntingtin (mHTT) protein (Q72 PC12 cells) was used as an in vitromodel of HD, while amyloid beta (A) treatment in mouse cortical neurons was used to mimic AD associated A toxicity in vitro. We found that FK866 in combination with nicotinic acid (NA) that maintains NAD levels while reducing NMN levels significantly rescued axonal pathology and ameliorated nuclear morphology in HD and AD cellular models.
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