{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE276nnn/GSE276656/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":[" Genome binding/occupancy profiling by high throughput sequencing","Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE276656"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Gene expression + ATAC multiome profiling of mPFC engram cells after OSK partial reprogramming","description":"Counteracting cognitive decline is an important goal in regenerative medicine. Recently, partial cellular reprogramming has emerged as a promising strategy to restore cellular function and promote tissue regeneration, but whether this approach can also reverse cognitive frailty is not known. In old mice and mouse models of Alzheimer’s Disease (AD) engram cells responsible for memory formation are functionally impaired, which prompted us to test the potential of their reprogramming to recover cognitive capacities. Here, by performing single nucleis multiome sequencing on the mPFC of the APP/PS1 AD mouse model, we found that partial reprogramming of its engram cells re-established aberrant epigenetic and transcriptional alterations.","dates":{"publication":"2026/02/10"},"accession":"GSE276656","cross_references":{"GSM":["GSM8503741","GSM8503730","GSM8503740","GSM8503734","GSM8503745","GSM8503744","GSM8503733","GSM8503743","GSM8503732","GSM8503742","GSM8503731","GSM8503738","GSM8503737","GSM8503748","GSM8503747","GSM8503736","GSM8503735","GSM8503746","GSM8503729","GSM8503739"],"GPL":["24247"],"GSE":["276656"],"taxon":["Mus musculus"],"PMID":["[41672073]"]}}