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Given that RNA modifications regulate neurodevelopment and neurodegeneration, we explore their functional role in 5xFAD mice, an A\u03b2 AD model. We discover that N1\u2010methyladenosine (m1A) is the most altered RNA modification, and that its regulator demethylase, ALKBH3 is upregulated. Strikingly,\n                    <jats:italic>Alkbh3<\/jats:italic>\n                    reduction decreases A\u03b2 plaques and restores cognition. Conversely, elevated ALKBH3 levels, observed in AD patients, compromise neuronal morphology and mitochondrial function by impairing mitophagy (degradation of dysfunctional mitochondria), a known driver of neuronal dysfunction. Mechanistically, we reveal that ALKBH3 removes m1A from PINK1 mRNA, the mitophagy master regulator. Given that ALKBH3 is elevated in human AD, causally linked to mitophagy impairment, and confers neuroprotection when depleted, we present ALKBH3 as a mechanistically validated therapeutic target in AD.\n                  <\/jats:p>","DOI":"10.1002\/advs.202522572","type":"journal-article","created":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T10:53:32Z","timestamp":1773312812000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["ALKBH3 m1A Demethylase Deficiency Reduces Alzheimer's Amyloid\u2010\u03b2 Pathology"],"prefix":"10.1002","volume":"13","author":[{"given":"Yueyang","family":"Li","sequence":"first","affiliation":[{"name":"Peking University  Beijing China"},{"name":"Beijing Institute for Brain Research Chinese Academy of Medical Sciences &amp; Peking Union Medical College  Beijing China"},{"name":"Chinese Institute for Brain Research, Beijing  Beijing 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