Although NMN has shown postive effects in clinical trials to date, there may be potential drawbacks in particular contexts. NMN’s interactions in neurological health warrant further investigation. NAD+ is also a cofactor for the enzyme sterile alpha and Toll/interleukin-1 receptor motif-containing 1 (SARM1), an enzyme that instigates neuronal degeneration after injury.[1] In people with neurological disorders and reduced activity of a specifc enzyme that converts NMN to NAD+ (nicotinamide mononucleotide adenylyltransferase 2, or NMNAT2), NMN supplementation could theoretically enhance neuron degeneration by increasing SARM1 activity.[2] However, in the context of healthy NMNAT2 enzyme activity, NMN supplementation could potentially be neuroprotective[3] Although more research is needed, it is safe to assume that NMN supplementation could have potential drawbacks in certain contexts, which warrants further study.
References
- ^Essuman K, Summers DW, Sasaki Y, Mao X, DiAntonio A, Milbrandt JThe SARM1 Toll/Interleukin-1 Receptor Domain Possesses Intrinsic NAD Cleavage Activity that Promotes Pathological Axonal Degeneration.Neuron.(2017-Mar-22)
- ^Figley MD, Gu W, Nanson JD, Shi Y, Sasaki Y, Cunnea K, Malde AK, Jia X, Luo Z, Saikot FK, Mosaiab T, Masic V, Holt S, Hartley-Tassell L, McGuinness HY, Manik MK, Bosanac T, Landsberg MJ, Kerry PS, Mobli M, Hughes RO, Milbrandt J, Kobe B, DiAntonio A, Ve TSARM1 is a metabolic sensor activated by an increased NMN/NAD ratio to trigger axon degeneration.Neuron.(2021-Apr-07)
- ^Thomas J Waller, Catherine A CollinsAn NAD+/NMN balancing act by SARM1 and NMNAT2 controls axonal degenerationNeuron.(2021 Apr 7)