<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/GSE268nnn/GSE268780/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Danio rerio</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=GSE268780</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Fibronectin mediates the interaction between vascular pathology and Alzheimer’s disease by inhibiting homeostatic gliovascular crosstalk</name><description>Alzheimer's disease (AD) often coexists with cerebrovascular pathology (CVP), contributing to cognitive decline and dementia. Understanding the molecular interplay between these pathologies is vital for developing effective therapies that can address the complexities of AD. The extracellular matrix (ECM) plays a crucial role in maintaining the blood-brain barrier (BBB) and modulating interactions of brain cell types with the vasculature. Elevated levels of a particular ECM component, Fibronectin 1 (FN1) are associated with both AD and vascular dysfunctions. In this study we show the molecular regulation exerted by FN1 to regulate the homeostatic interaction between vasculature and the brain.</description><dates><publication>2026/07/02</publication></dates><accession>GSE268780</accession><cross_references><GSM>GSM8299023</GSM><GSM>GSM8299022</GSM><GPL>20828</GPL><GSE>268780</GSE><taxon>Danio rerio</taxon></cross_references></HashMap>