NAD plus Modulates the Proliferation and Differentiation of Adult Neural Stem/Progenitor Cells via Akt Signaling Pathway

Nicotinamide adenine dinucleotide hydrate (NAD+) acts as the essential component of the tricarboxylic citric acid (TCA) cycle and has important functions in diverse biological processes. However, the roles of NAD+ in regulating adult neural stem/progenitor cells (aNSPCs) remain largely unknown. Here, we show that NAD+ exposure leads to the reduced proliferation and neuronal differentiation of aNSPCs and induces the apoptosis of aNSPCs. In addition, NAD+ exposure inhibits the morphological development of neurons. Mechanistically, RNA sequencing revealed that the transcriptome of aNSPCs is altered by NAD+ exposure. NAD+ exposure significantly decreases the expression of multiple genes related to ATP metabolism and the PI3k-Akt signaling pathway. Collectively, our findings provide some insights into the roles and mechanisms in which NAD+ regulates aNSPCs and neuronal development.

Automated summary

Nicotinamide adenine dinucleotide hydrate (NAD+) plays a crucial role in regulating adult neural stem/progenitor cells (aNSPCs) by reducing proliferation, neuronal differentiation, and inducing apoptosis. NAD+ exposure also inhibits neuronal morphological development. Mechanistically, NAD+ exposure alters transcriptome and decreases the expression of genes related to ATP metabolism and the PI3k-Akt signaling pathway.