<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/GSE315nnn/GSE315336/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE315336</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Compartment specific mitochondrial unfolded protein response</name><description>Alzheimer’s disease lacks effective disease‑modifying treatments partly because early, compartment‑specific mitochondrial stress responses in microglia remain poorly defined. Our findings show that APP expression and targeted activation of UPRmt-MM or UPRmt-IMS produce distinct transcriptional signatures—ranging from immune activation and impaired oxidative phosphorylation to disrupted mitochondrial ribosome integrity—highlighting mitochondrial compartmentalization as a key driver of AD pathogenesis and a potential therapeutic target.</description><dates><publication>2026/09/09</publication></dates><accession>GSE315336</accession><cross_references><GSM>GSM9425570</GSM><GSM>GSM9425572</GSM><GSM>GSM9425561</GSM><GSM>GSM9425560</GSM><GSM>GSM9425571</GSM><GSM>GSM9425563</GSM><GSM>GSM9425574</GSM><GSM>GSM9425562</GSM><GSM>GSM9425573</GSM><GSM>GSM9425565</GSM><GSM>GSM9425564</GSM><GSM>GSM9425567</GSM><GSM>GSM9425566</GSM><GSM>GSM9425569</GSM><GSM>GSM9425568</GSM><GSM>GSM9425559</GSM><GPL>11154</GPL><GSE>315336</GSE><taxon>Homo sapiens</taxon><PMID>[42694256]</PMID></cross_references></HashMap>