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AD is characterized by the accumulation and aggregation of misfolded proteins in brain, the sustained activation of the UPR mediated by the misfold proteins initiates or mediates neurodegeneration (Hoozemans et al., 2005)

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The same authors also showed [59, 70] that the action of both CAT and GPx was insufficient to explain the erythrocyte oxidative catabolism, and proposed [70] a model including Prx2 that, in accordance with their experimental data, could better explain the erythrocyte antioxidant defense system

Neurological research applications are emerging as scientists recognize the connections between NNMT, NAD+ metabolism and neuronal function