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Several membrane-bound proteins suggested to play a role in this process include CD73, able to convert NMN into NR 67 , and NAD + glycohydrolases such as CD38 that convert NAD + into NAM and ADP-ribose

It reacts with cysteine and methionine amino acid side chains causing protein damage

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This oxidant stress causes activation of a MAP kinase cascade in the cytosol ultimately leading to phosphorylation of c-jun N-terminal kinase (P-JNK), translocation of P-JNK to the mitochondria [34], and binding to the anchor protein Sab [35] for amplification of the mitochondrial oxidant stress and peroxynitrite formation in the mitochondrial matrix [33, 36]

As such, secondary outcomes include changes in cognition, disease severity and function before and after treatment and across the one-year study period and measures of senescence and AD biomarkers in CSF pre- and post-treatment (baseline and three months) with an optional end of study collection