{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T09:04:19Z","timestamp":1789376659824,"version":"build-2803163510"},"reference-count":110,"publisher":"Wiley","issue":"51","license":[{"start":{"date-parts":[[2026,6,25]],"date-time":"2026-06-25T00:00:00Z","timestamp":1782345600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,6,25]],"date-time":"2026-06-25T00:00:00Z","timestamp":1782345600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","award":["R01AG086365 to T.L R21AG070299 to T.L R21AG095389 to T.L R03AG084948 to T.L"],"award-info":[{"award-number":["R01AG086365 to T.L R21AG070299 to T.L R21AG095389 to T.L R03AG084948 to T.L"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["RF1NS133812"],"award-info":[{"award-number":["RF1NS133812"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["advanced.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Advanced Science"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Mitochondrial dysfunction and chromatin dysregulation are interconnected contributors to neuronal vulnerability in Alzheimer's disease (AD), yet the molecular mechanisms linking these processes remain poorly understood. CHCHD10, a mitochondrial intermembrane space protein, has been implicated in neurodegenerative disorders, but its role in AD has not been defined. Here, we identify CHCHD10 as a previously unrecognized modulator of neuronal epigenomic stability in AD. Using direct fibroblast\u2010to\u2010neuron reprogramming, which preserves patient\u2010specific epigenetic signatures, we show that AD neurons recapitulate genome\u2010wide hypomethylation patterns observed in postmortem AD cortex. CHCHD10 expression is significantly reduced in AD neurons and across multiple human brain datasets, including single\u2010cell and bulk RNA sequencing, proteomics, and human cortical tissue analyses. Restoration of CHCHD10 in AD neurons reduces amyloid\u2010\u03b2 and insoluble tau accumulation while reversing AD\u2010associated differentially methylated regions across CpG islands, promoters, and regulatory elements. CHCHD10\u2010responsive methylation changes overlap with those observed in human AD brain regions and colocalize with significant AD loci and cortex\u2010specific eQTL loci, including MAPT and ABCA7. Finally, we identify KATNAL2 as a CHCHD10\u2010responsive effector whose loss enhances tau phosphorylation and seeding, whereas its restoration mitigates tau pathology. Together, these findings support a CHCHD10\u2010associated neuroprotective pathway linking mitochondrial dysfunction, epigenomic instability, and tau pathology in AD.<\/jats:p>","DOI":"10.1002\/advs.76205","type":"journal-article","created":{"date-parts":[[2026,6,25]],"date-time":"2026-06-25T16:24:44Z","timestamp":1782404684000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["CHCHD10 Mitigates Alzheimer's Disease\u2010Related Phenotypes in Association With Epigenetic Remodeling in Directly Reprogrammed Neurons"],"prefix":"10.1002","volume":"13","author":[{"given":"Teresa M.","family":"Thomas","sequence":"first","affiliation":[{"name":"Department of Pathology Case Western Reserve University School of Medicine  Cleveland Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ching\u2010Yao","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Pathology Case Western Reserve 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