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Background  The  Wld S   mouse mutant ("Wallerian degeneration-slow") delays axonal degeneration in a variety of disorders including  in vivo  models of Parkinson's disease. The mechanisms underlying  Wld S   -mediated axonal protection are unclear, although many studies have attributed  Wld S   neuroprotection to the NAD + -synthesizing Nmnat1 portion of the fusion protein. Here, we used dissociated dopaminergic cultures to test the hypothesis that catalytically active Nmnat1 protects dopaminergic neurons from toxin-mediated axonal injury.    Results  Using mutant mice and lentiviral transduction of dopaminergic neurons, the present findings demonstrate that  Wld S   but not Nmnat1, Nmnat3, or cytoplasmically-targeted Nmnat1 protects dopamine axons from the parkinsonian mimetic N-methyl-4-phenylpyridinium (MPP + ). Moreover, NAD +  synthesis is not required since enzymatically-inactive  Wld S   still protects. In addition, NAD +  by itself is axonally protective and together with  Wld S   is additive in the MPP +  model.    Conclusions  Our data suggest that NAD +  and  Wld S   act through separate and possibly parallel mechanisms to protect dopamine axons. As MPP +  is thought to impair mitochondrial function, these results suggest that  Wld S   might be involved in preserving mitochondrial health or maintaining cellular metabolism.

WldS but not Nmnat1 protects dopaminergic neurites from MPP+ neurotoxicity