As a complex neurodegenerative disease, the pathogenesis of Alzheimer’s disease (AD) has not been fully elucidated. This article reviews the role and regulatory mechanism of m⁶A modification in AD, with the aim of exploring how m⁶A modification participates in the pathological process of AD by regulating the “writer”, “eraser”, and “reader” proteins, and evaluating its potential in diagnosis, treatment, and prognosis. This article systematically summarizes the regulatory mechanisms of m⁶A modification on amyloid metabolism, Tau protein phosphorylation, neuronal apoptosis, synaptic function, and neuroinflammation, and reviews the research progress on m⁶A-related biomarkers and targeted therapy strategies. The results indicate that abnormal levels of m⁶A modification and related enzyme expression in brain tissue and peripheral blood of AD patients lead to metabolic disorders of key genes such as APP, BACE1, and MAPT mRNA, which promote A β deposition and Tau pathology, while exacerbating neuronal damage and neuroinflammation. In addition, peripheral blood m⁶A regulatory factors and modification sites can serve as potential biomarkers for early diagnosis and prognostic evaluation of Alzheimer’s disease, and targeted therapy strategies targeting METTL3, FTO, and non-coding RNA have shown promising application prospects. The conclusion is that in-depth analysis of the dynamic regulatory network modified by m⁶A is expected to provide new ideas and targets for early diagnosis, precise treatment, and prognosis improvement of AD.