{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Andrew RJ"],"funding":["HHS | National Institutes of Health","NIA NIH HHS","Illinois Department of Public Health","BrightFocus Foundation","Cure Alzheimer&apos;s Fund","Alzheimer&apos;s Association","HHS | NIH | National Institute on Aging","NIH HHS"],"pagination":["4477-4487"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6433054"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["294(12)"],"pubmed_abstract":["Alzheimer's disease (AD) is pathologically characterized by the deposition of the β-amyloid (Aβ) peptide in senile plaques in the brain, leading to neuronal dysfunction and eventual decline in cognitive function. Genome-wide association studies have identified the <i>bridging integrator 1</i> (<i>BIN1</i>) gene within the second most significant susceptibility locus for late-onset AD. BIN1 is a member of the amphiphysin family of proteins and has reported roles in the generation of membrane curvature and endocytosis. Endocytic dysfunction is a pathological feature of AD, and endocytosis of the amyloid precursor protein is an important step in its subsequent cleavage by β-secretase (BACE1). <i>In vitro</i> evidence implicates BIN1 in endosomal sorting of BACE1 and Aβ generation in neurons, "],"journal":["The Journal of biological chemistry"],"pubmed_title":["Reduction of the expression of the late-onset Alzheimer's disease (AD) risk-factor <i>BIN1</i> does not affect amyloid pathology in an AD mouse model."],"pmcid":["PMC6433054"],"funding_grant_id":["83282004F","RF1 AG054223","AG056061","AARF-17–501228","16477","S10 OD010649","AG054223","A2017366F","RF1 AG056061","S10OD010649"],"pubmed_authors":["Guerbette T","Andrew RJ","Rice RC","Wagner SL","De Rossi P","Thinakaran G","Recupero AJ","Nguyen P","Kowalski HR","Laury-Kleintop L","Krause SV"],"additional_accession":[]},"is_claimable":false,"name":"Reduction of the expression of the late-onset Alzheimer's disease (AD) risk-factor <i>BIN1</i> does not affect amyloid pathology in an AD mouse model.","description":"Alzheimer's disease (AD) is pathologically characterized by the deposition of the β-amyloid (Aβ) peptide in senile plaques in the brain, leading to neuronal dysfunction and eventual decline in cognitive function. Genome-wide association studies have identified the <i>bridging integrator 1</i> (<i>BIN1</i>) gene within the second most significant susceptibility locus for late-onset AD. BIN1 is a member of the amphiphysin family of proteins and has reported roles in the generation of membrane curvature and endocytosis. Endocytic dysfunction is a pathological feature of AD, and endocytosis of the amyloid precursor protein is an important step in its subsequent cleavage by β-secretase (BACE1). <i>In vitro</i> evidence implicates BIN1 in endosomal sorting of BACE1 and Aβ generation in neurons, ","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Mar","modification":"2026-05-03T14:19:41.696Z","creation":"2026-04-07T19:19:14.893Z"},"accession":"S-EPMC6433054","cross_references":{"pubmed":["30692199"],"doi":["10.1074/jbc.RA118.006379","10.1074/jbc.ra118.006379"]}}