{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yu X"],"funding":["Guangdong Province Special Fund for Science and Technology Project","National Natural Science Foundation of China","Natural Science Foundation of Guang-dong Province","National Science and Technology Major Project","Guangdong Science and Technology Plan Projects"],"pagination":["30134"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12358618"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"pubmed_abstract":["Alzheimer's disease (AD) is a major cause of dementia, characterized by β-amyloid (Aβ) plaque accumulation and Tau protein hyperphosphorylation. Although long non-coding RNAs (lncRNAs) have been implicated in neurodegenerative diseases, their roles in AD remain unclear. This study analyzed RNA sequencing data from the brain tissues of 17 AD patients and 19 healthy controls (GEO: GSE138260) to construct a gene co-expression network and identified eight lncRNAs strongly associated with AD. FMR1-AS1 was selected for functional validation. In an Aβ1-42-induced SH-SY5Y neuronal injury model, overexpression of FMR1-AS1 significantly increased cell viability ([Formula: see text]), inhibited apoptosis ([Formula: see text]), and reduced Tau hyperphosphorylation ([Formula: see text]). FMR1-AS1 also "],"journal":["Scientific reports"],"pubmed_title":["Regulatory role of LncRNA FMR1-AS1 in the pathogenesis of alzheimer's disease based on bioinformatics and in vitro experimental validation."],"pmcid":["PMC12358618"],"funding_grant_id":["STKJ202209017","2024ZD0529106","62002212","STKJ2023012","2025A1515012810"],"pubmed_authors":["He C","Li Y","Chen L","Ouyang Z","Yu X","Cai H"],"additional_accession":[]},"is_claimable":false,"name":"Regulatory role of LncRNA FMR1-AS1 in the pathogenesis of alzheimer's disease based on bioinformatics and in vitro experimental validation.","description":"Alzheimer's disease (AD) is a major cause of dementia, characterized by β-amyloid (Aβ) plaque accumulation and Tau protein hyperphosphorylation. Although long non-coding RNAs (lncRNAs) have been implicated in neurodegenerative diseases, their roles in AD remain unclear. This study analyzed RNA sequencing data from the brain tissues of 17 AD patients and 19 healthy controls (GEO: GSE138260) to construct a gene co-expression network and identified eight lncRNAs strongly associated with AD. FMR1-AS1 was selected for functional validation. In an Aβ1-42-induced SH-SY5Y neuronal injury model, overexpression of FMR1-AS1 significantly increased cell viability ([Formula: see text]), inhibited apoptosis ([Formula: see text]), and reduced Tau hyperphosphorylation ([Formula: see text]). FMR1-AS1 also ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Aug","modification":"2026-05-29T14:42:44.138Z","creation":"2026-04-08T05:07:00.826Z"},"accession":"S-EPMC12358618","cross_references":{"pubmed":["40820106"],"doi":["10.1038/s41598-025-15242-y"]}}