<p>RNA metabolic dysregulation is a key pathological mechanism underlying the onset and progression of Alzheimer’s disease (AD), involving multiple aspects such as abnormal RNA splicing, loss of function in RNA-binding proteins, dysregulation of non-coding RNAs, and impaired nuclear-cytoplasmic transport. In recent years, the emergence of epigenome research has revealed the critical role of RNA chemical modifications in regulating RNA metabolism at the post-transcriptional level. N4-acetylcytidine (ac4C) is the only known RNA acetylation modification in eukaryotes and is specifically catalyzed by N-acetyltransferase 10 (NAT10). The ac4C modification is widely found in tRNA, rRNA, and mRNA, and by influencing RNA stability, translation efficiency, and ribosome assembly, it participates in various biological processes such as the cell cycle, differentiation, aging, and stress responses. In AD, the ac4C modification profile undergoes significant changes, involving GABAergic synapses, the PI3K-AKT signaling pathway, and various lncRNAs. Although indirect evidence from progeria and tumor models suggests that via α-tubulin acetylation and intersect with AD pathology via the p53 pathway and regulation of autophagy, these mechanisms currently lack direct experimental validation in NAT10 may participate in axonal transport through α-tubulin acetylation and intersect with AD pathology via the p53 pathway and autophagy regulation, these mechanisms currently lack direct experimental validation within the AD system. This article systematically summarizes the molecular basis and regulatory networks of ac4C modification, integrates existing evidence and unresolved questions regarding its role in AD, and explores its potential value as a diagnostic biomarker and therapeutic target, with the aim of providing guidance for future research in this field.</p>