Beneficial Effect of NMN on the Maintenance of Neuritic Arbor in Motor Neurons

Introduction

Replenishing nicotinamide mononucleotide (NMN) to raise the availability of nicotinamide adenine dinucleotide (NAD+) has been deemed as effective approach to prevent neurodegeneration in aging and pathological conditions including ALS, a fatal progressive neurodegenerative disorder with no known way to cure.


 

The association of SOD1 and TDP-43 with ALS

Cu/Zn-superoxide dismutase (SOD1) is the first identified protein associated with familial ALS. In most ALS cases, Transactive Response DNA Binding Protein 43 (TDP-43) pathology is frequently observed. Both SOD1 and TDP-43 have tight association with motor neuron degeneration in patients with ALS. Mutant SOD1 could affect the solubility/insolubility of TDP-43 through physical interactions. Mutant SOD1^G93A and the fragment form of TDP-43 can exert synergistic effect to mediate toxic events in apoptosis.

The protective effect of NMN on motor neurons

NMN can increase the neurite length and complexity in mouse motor neurons and iPSC-derived human motor neurons overexpressing wild-type TDP-43/mutant hSOD1^G93A. Meanwhile, it prevents the neuronal death and the increased nitro-tyrosine immunoreactivity induced by trophic factor deprivation. In motor neurons overexpressing mutant hSOD1^G93A, the neuroprotection conferred by NMN supplementation is mediated by a mechanism that involves an increase in glutathione content. However, this neuroprotective effect does not involve the alteration of glutathione content in non-transgenic or TDP-43 overexpressing motor neurons.

The involvement of TDP-43 pathology in ALS

NMN supplementation can confer axonal protection in motor neurons isolated from two dissimilar models of ALS, with and without involvement of TDP-43 pathology. Besides, NMN treatment can correct the morphological changes induced by TDP-43 overexpression in motor neurons and boost the nuclear localization of TDP-43 and phosphorylated TDP-43, which favors its nuclear localization and averts the detrimental effects of TDP-43 overexpression on neurite length and complexity.

Conclusion

Reference

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