Dynamic m⁶A Methylation in Neurodevelopmental and Neurodegenerative Disorders

N⁶-methyladenosine (m⁶A), the most prevalent internal modification in eukaryotic RNA, has emerged as a key epitranscriptomic regulator in the central nervous system, coordinating gene expression programs that govern neural development, synaptic plasticity, and neuronal adaptation throughout the lifespan. This review synthesizes emerging evidence that m⁶A dysregulation represents a shared epitranscriptomic mechanism linking neurodevelopmental and neurodegenerative disorders, highlighting a mechanistic convergence that bridges these traditionally distinct disease categories. Dysregulation of m⁶A-mediated control of neurogenesis, synaptic maturation, and dopaminergic development has been implicated in neurodevelopmental disorders, including autism spectrum disorder, attention-deficit/hyperactivity disorder, and intellectual disability. In neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease, m⁶A dysregulation mediates multiple interconnected pathogenic processes, including neuroinflammation, mitochondrial dysfunction, tau hyperphosphorylation and aggregation, α-synuclein dysregulation, and impaired neuronal repair. Environmental stressors and metabolic perturbations modulate m⁶A modification patterns, suggesting that gene-environment interactions contribute to disease susceptibility through epitranscriptomic mechanisms. m⁶A modification functions as a dynamic molecular switch governing neural plasticity and circuit function across early development, adulthood, and aging, and its dysregulation predisposes individuals to neurological disease manifestation throughout the lifespan. Advances in cell-type-specific and circuit-resolved m⁶A profiling will deepen our understanding of m⁶A dysregulation and strengthen its translational potential as both a diagnostic biomarker and a therapeutic target in neurological diseases. Furthermore, we evaluate pharmacological and molecular strategies targeting m⁶A regulatory machinery, including the writers METTL3/METTL14, the erasers FTO/ALKBH5, and reader proteins, as promising therapeutic approaches to restore aberrant neuronal circuit function in neurodevelopmental and neurodegenerative disorders.