Abstract: Ischemic stroke (IS) is a major disease leading to death and disability, with currently limited clinical treatment options. Adult hippocampal neurogenesis mediated by endogenous neural stem cells (NSCs) offers a new therapeutic strategy for neurological functional recovery after IS. N6-methyladenosine (m⁶A), the most prevalent internal chemical modification in eukaryotic mRNA, dynamically regulates gene expression through its "writers, " "erasers, " and "readers." Studies have shown that m⁶A modification plays a central role in maintaining the balance between quiescence and proliferation of hippocampal NSCs, determining their differentiation fate, and promoting the maturation and integration of newborn neurons. Following IS, m⁶A modification levels and the expression of related enzymes in the brain undergo significant changes. These alterations may influence various stages of neurogenesis by regulating RNA metabolism, thereby affecting brain damage repair and cognitive functional recovery. This article systematically reviews the molecular mechanisms by which m⁶A modification regulates adult hippocampal neurogenesis, outlines the dynamic changes in m⁶A modification in the brain after IS, and proposes the hypothesis that m⁶A may serve as a key molecular hub linking ischemic brain injury and adult hippocampal neurogenesis. Finally, this article analyzes the core limitations of current research and discusses future research directions from the perspectives of technological development and clinical translation.