{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T23:23:52Z","timestamp":1793316232793,"version":"4.5.0"},"reference-count":316,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","license":[{"start":{"date-parts":[[2025,7,5]],"date-time":"2025-07-05T00:00:00Z","timestamp":1751673600000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0 http:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,6]]},"abstract":"\n N\n 6<\/jats:sup>\n -methyladenosine RNA methylation, an essential post-transcriptional modification, dynamically regulates RNA metabolism and plays a crucial role in neuronal function. Growing evidence suggests that dysregulated N\n 6<\/jats:sup>\n -methyladenosine modification contributes to the pathogenesis of neurodegenerative diseases, including Alzheimer\u2019s disease, Parkinson\u2019s disease, multiple sclerosis, and amyotrophic lateral sclerosis. However, the precise mechanisms by which N\n 6<\/jats:sup>\n -methyladenosine modification influences these conditions remain unclear. This review summarizes the role of m\n 6<\/jats:sup>\n A modification and its associated regulators in neurodegeneration, focusing on their involvement in key pathological processes. In Alzheimer\u2019s disease, m\n 6<\/jats:sup>\n A modification contributes to synaptic dysfunction, mitochondrial damage, and neuronal apoptosis. Evidence from APP\/PS1, 5xFAD, tau transgenic, and\n Drosophila<\/jats:italic>\n models demonstrates that regulators such as methyltransferase-like 3 and fat mass and obesity-associated protein influence Alzheimer\u2019s disease progression through neuroinflammation, circular RNAs dysregulation, and autophagy-related mechanisms. In Parkinson\u2019s disease, altered N\n 6<\/jats:sup>\n -methyladenosine regulator expression affects dopaminergic neuron survival and stress responses by modulating mRNA stability and autophagy-related lncRNAs. In multiple sclerosis and amyotrophic lateral sclerosis, N\n 6<\/jats:sup>\n -methyladenosine affects immune activation, myelin repair, and the regulation of disease-associated genes such as\n TDP-43<\/jats:italic>\n . Beyond N\n 6<\/jats:sup>\n -methyladenosine, other RNA methylation modifications\u2014such as m\n 1<\/jats:sup>\n A, m\n 5<\/jats:sup>\n C, m\n 7<\/jats:sup>\n G, uracil, and pseudouridine\u2014are implicated in neurodegenerative diseases through their regulation of mitochondrial function, RNA metabolism, and neuronal stress responses. Additionally, N\n 6<\/jats:sup>\n -methyladenosine exhibits cell type\u2013specific functions: in microglia, it regulates inflammatory activation and phagocytic function; in astrocytes, it modulates metabolic homeostasis and glutamate-associated neurotoxicity; in neurons, it affects synaptic function and neurodegeneration-related gene expression; and in adult neural stem cells, it controls differentiation, neurogenesis, and cognitive plasticity. Recently, several small-molecule inhibitors targeting methyltransferase-like 3 or fat mass and obesity-associated protein have been developed to modulate N\n 6<\/jats:sup>\n -methyladenosine modification, providing new opportunities for disease intervention, with the targeting of N\u2076-methyladenosine-related pathways emerging as a promising therapeutic strategy. However, challenges persist in optimizing the specificity and delivery of these therapeutic approaches.\n <\/jats:p>","DOI":"10.4103\/nrr.nrr-d-24-01648","type":"journal-article","created":{"date-parts":[[2025,7,6]],"date-time":"2025-07-06T08:00:14Z","timestamp":1751788814000},"page":"2191-2204","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":10,"title":["Neuromodulatory role and therapeutic potential of N6-methyladenosine RNA methylation in neurodegenerative diseases"],"prefix":"10.4103","volume":"21","author":[{"given":"Jinyu","family":"Zhang","sequence":"first","affiliation":[{"name":"Hengyang Medical School, University of South China, Hengyang, Hunan Province, China"},{"name":"Brain Science Center, Beijing Institute of Basic Medical Sciences, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenjing","family":"Ma","sequence":"additional","affiliation":[{"name":"Hengyang Medical School, University of South China, Hengyang, Hunan Province, China"},{"name":"Brain Science Center, Beijing Institute of Basic Medical Sciences, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ranxu","family":"Liu","sequence":"additional","affiliation":[{"name":"Hengyang Medical School, University of South China, Hengyang, Hunan Province, China"},{"name":"Brain Science Center, Beijing Institute of Basic Medical Sciences, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoheng","family":"Li","sequence":"additional","affiliation":[{"name":"Brain Science Center, Beijing Institute of Basic Medical Sciences, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5739-2867","authenticated-orcid":false,"given":"Zengqiang","family":"Yuan","sequence":"additional","affiliation":[{"name":"Brain Science Center, Beijing Institute of Basic Medical Sciences, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3627-8544","authenticated-orcid":false,"given":"Jinbo","family":"Cheng","sequence":"additional","affiliation":[{"name":"Brain Science Center, Beijing Institute of Basic Medical Sciences, Beijing, China"},{"name":"Center on Translational Neuroscience, College of Life & Environmental Science, Minzu University of China, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2025,7,5]]},"reference":[{"key":"R1-20260416","doi-asserted-by":"crossref","first-page":"19071","DOI":"10.1038\/s41598-019-55742-2","article-title":"The FTO gene polymorphism rs9939609 is associated with obesity and disability in multiple sclerosis patients","volume":"9","author":"Al-Serri","year":"2019","journal-title":"Sci 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