N6-methyladenosine (m⁶A), the most abundant modification in messenger RNAs (mRNAs), is deposited by methyltransferases (“writers”) Mettl3 and Mettl14 and erased by demethylases (“erasers”) Fto and Alkbh5. m⁶A can be recognized by m⁶A-binding proteins (“readers”), such as Yth domain family proteins (Ythdfs) and Yth domain-containing protein 1 (Ythdc1). Previous studies have indicated that m⁶A plays an essential function in various fundamental biological processes, including neurogenesis and neuronal development. Dysregulated m⁶A modification contributes to neurological disorders, including neurodegenerative diseases. In this review, we summarize the current knowledge about the roles of m⁶A machinery, including writers, erasers, and readers, in regulating gene expression and the function of m⁶A in neurodevelopment and neurodegeneration. We also discuss the perspectives for studying m⁶A methylation.

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.