Objective: To explore the core role of N6-methyladenosine (m6A) methylation in neurodegenerative cognitive disorders, with a particular focus on its contribution to disease progression through the regulation of common mechanisms such as neuroimmune inflammation, and to discuss its clinical translational prospects. Methods: A systematic review of recent research literature on m6A methylation in neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease, was conducted, integrating analyses from molecular mechanisms, cellular phenotypes, to systemic pathology. Results and Conclusions: As a key epitranscriptomic regulatory mechanism, m6A methylation precisely regulates neural synaptic plasticity, autophagic clearance, and neuroimmune homeostasis through a dynamic network comprising “writer”, “eraser”, and “reader” proteins. Its homeostatic imbalance represents a core pathological hub leading to cognitive dysfunction: on one hand, m6A dysregulation directly mediates the polarization of microglia towards a pro-inflammatory M1 phenotype, amplifying neuroinflammatory responses; on the other hand, it exacerbates neuronal injury by affecting the metabolism of pathological proteins such as Tau and α-synuclein. Targeting m6A regulatory enzymes (e.g., FTO inhibitors, METTL3 activators) has shown potential for improving cognitive function in preclinical models. Additionally, biomarkers like m6A in peripheral blood exosomes hold value for non-invasive diagnosis. In summary, m6A methylation serves as a critical link connecting common pathological mechanisms across various neurodegenerative diseases, offering broad translational application prospects in disease diagnosis and targeted therapy.