<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE328nnn/GSE328184/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><omics_type>Methylation profiling</omics_type><species>Homo sapiens</species><gds_type>Methylation profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE328184</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>CHCHD10 alleviates Alzheimer’s Disease Pathogenesis by Modulating Epigenetic Landscape in Directly Reprogrammed Neurons</name><description>Alzheimer’s disease (AD) is associated with widespread epigenetic alterations, including changes in DNA methylation. CHCHD10, a mitochondrial intermembrane space protein, has been implicated in mitochondrial function and neurodegeneration, but its role in epigenetic regulation remains unclear. In this study, we performed genome-wide DNA methylation profiling in fibroblast-derived induced neurons from cognitively normal controls (NC) and AD patients, with and without CHCHD10 overexpression. We identified disease-associated differentially methylated regions (DMRs) and evaluated the extent to which CHCHD10 restoration modulates these epigenetic signatures. This dataset provides a resource for understanding mitochondrial-epigenetic interactions in AD.</description><dates><publication>2026/06/29</publication></dates><accession>GSE328184</accession><cross_references><GSM>GSM9674590</GSM><GSM>GSM9674592</GSM><GSM>GSM9674591</GSM><GSM>GSM9674594</GSM><GSM>GSM9674593</GSM><GSM>GSM9674596</GSM><GSM>GSM9674595</GSM><GSM>GSM9674598</GSM><GSM>GSM9674597</GSM><GSM>GSM9674589</GSM><GSM>GSM9674588</GSM><GSM>GSM9674599</GSM><GPL>24676</GPL><GSE>328184</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>