Nicotinamide adenine dinucleotide (NAD+), a coenzyme involved in redox activities in the mitochondrial electron transport chain, has been identified as a key regulator of the lifespan-extending effects, and the activation of NAD expression has been linked with a decrease in beta-amyloid (Ab) toxicity in Alzheimer’s disease (AD).
Nicotinamide riboside (NR) is a NAD precursor, it promotes peroxisome proliferator- activated receptor-g coactivator 1 (PGC)-1α expression in the brain. Evidence has shown that PGC-1α is a crucial regulator of Ab generation because it affects b-secretase (BACE1) degradation.
NR naturally occurs in yeast, bacteria, and mammals, and is present in milk and beer. It is metabolized by two metabolic pathways. The first is a degradative pathway that produces nicotinamide. The second pathway involves NR kinases. Through those pathways, NR is converted to NAD+.
