<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hamilton HL</submitter><funding>National Institute of Neurological Disorders and Stroke</funding><funding>NINDS NIH HHS</funding><funding>NCI NIH HHS</funding><funding>NIH HHS</funding><pagination>1607-1625</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10828232</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>46(2)</volume><pubmed_abstract>Alzheimer's disease (AD), the most common cause of dementia in the elderly, is characterized by the accumulation of intracellular neurofibrillary tangles, extracellular amyloid plaques, and neuroinflammation. In partnership with microglial cells, astrocytes are key players in the regulation of neuroinflammation. Fatty acid binding protein 7 (FABP7) belongs to a family of conserved proteins that regulate lipid metabolism, energy homeostasis, and inflammation. FABP7 expression is largely restricted to astrocytes and radial glia-like cells in the adult central nervous system. We observed that treatment of primary hippocampal astrocyte cultures with amyloid β fragment 25-35 (Aβ&lt;sub>25-35&lt;/sub>) induces FABP7 upregulation. In addition, FABP7 expression is upregulated in the brain of APP/PS1 mic</pubmed_abstract><journal>GeroScience</journal><pubmed_title>FABP7 drives an inflammatory response in human astrocytes and is upregulated in Alzheimer's disease.</pubmed_title><pmcid>PMC10828232</pmcid><funding_grant_id>R01NS122973</funding_grant_id><funding_grant_id>S10 OD023526</funding_grant_id><funding_grant_id>P30 CA014520</funding_grant_id><funding_grant_id>R01 NS122973</funding_grant_id><pubmed_authors>Balmer G</pubmed_authors><pubmed_authors>Kinscherf NA</pubmed_authors><pubmed_authors>Pehar M</pubmed_authors><pubmed_authors>Vargas MR</pubmed_authors><pubmed_authors>Salamat SM</pubmed_authors><pubmed_authors>Bresque M</pubmed_authors><pubmed_authors>Hamilton HL</pubmed_authors></additional><is_claimable>false</is_claimable><name>FABP7 drives an inflammatory response in human astrocytes and is upregulated in Alzheimer's disease.</name><description>Alzheimer's disease (AD), the most common cause of dementia in the elderly, is characterized by the accumulation of intracellular neurofibrillary tangles, extracellular amyloid plaques, and neuroinflammation. In partnership with microglial cells, astrocytes are key players in the regulation of neuroinflammation. Fatty acid binding protein 7 (FABP7) belongs to a family of conserved proteins that regulate lipid metabolism, energy homeostasis, and inflammation. FABP7 expression is largely restricted to astrocytes and radial glia-like cells in the adult central nervous system. We observed that treatment of primary hippocampal astrocyte cultures with amyloid β fragment 25-35 (Aβ&lt;sub>25-35&lt;/sub>) induces FABP7 upregulation. In addition, FABP7 expression is upregulated in the brain of APP/PS1 mic</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Apr</publication><modification>2026-06-02T11:22:58.724Z</modification><creation>2025-04-05T12:46:39.226Z</creation></dates><accession>S-EPMC10828232</accession><cross_references><pubmed>37688656</pubmed><doi>10.1007/s11357-023-00916-0</doi></cross_references></HashMap>