{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["M Leite D"],"funding":["European Research Council","Engineering and Physical Sciences Research Council"],"pagination":["fcac039"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8882007"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["4(1)"],"pubmed_abstract":["A deficient transport of amyloid-β across the blood-brain barrier, and its diminished clearance from the brain, contribute to neurodegenerative and vascular pathologies, such as Alzheimer's disease and cerebral amyloid angiopathy, respectively. At the blood-brain barrier, amyloid-β efflux transport is associated with the low-density lipoprotein receptor-related protein 1. However, the precise mechanisms governing amyloid-β transport across the blood-brain barrier, in health and disease, remain to be fully understood. Recent evidence indicates that the low-density lipoprotein receptor-related protein 1 transcytosis occurs through a tubulation-mediated mechanism stabilized by syndapin-2. Here, we show that syndapin-2 is associated with amyloid-β clearance via low-density lipoprotein receptor-related protein 1 across the blood-brain barrier. We further demonstrate that risk factors for Alzheimer's disease, amyloid-β expression and ageing, are associated with a decline in the native expression of syndapin-2 within the brain endothelium. Our data reveals that syndapin-2-mediated pathway, and its balance with the endosomal sorting, are important for amyloid-β clearance proposing a measure to evaluate Alzheimer's disease and ageing, as well as a target for counteracting amyloid-β build-up. Moreover, we provide evidence for the impact of the avidity of amyloid-β assemblies in their trafficking across the brain endothelium and in low-density lipoprotein receptor-related protein 1 expression levels, which may affect the overall clearance of amyloid-β across the blood-brain barrier."],"journal":["Brain communications"],"pubmed_title":["Syndapin-2 mediated transcytosis of amyloid-β across the blood-brain barrier."],"pmcid":["PMC8882007"],"funding_grant_id":["EP/N026322/1","769798","EP/I001697/1","278793"],"pubmed_authors":["Seifi M","Battaglia G","Swinny JD","Plomann M","Ruiz-Perez L","Nguemo F","M Leite D"],"additional_accession":[]},"is_claimable":false,"name":"Syndapin-2 mediated transcytosis of amyloid-β across the blood-brain barrier.","description":"A deficient transport of amyloid-β across the blood-brain barrier, and its diminished clearance from the brain, contribute to neurodegenerative and vascular pathologies, such as Alzheimer's disease and cerebral amyloid angiopathy, respectively. At the blood-brain barrier, amyloid-β efflux transport is associated with the low-density lipoprotein receptor-related protein 1. However, the precise mechanisms governing amyloid-β transport across the blood-brain barrier, in health and disease, remain to be fully understood. Recent evidence indicates that the low-density lipoprotein receptor-related protein 1 transcytosis occurs through a tubulation-mediated mechanism stabilized by syndapin-2. Here, we show that syndapin-2 is associated with amyloid-β clearance via low-density lipoprotein receptor-related protein 1 across the blood-brain barrier. We further demonstrate that risk factors for Alzheimer's disease, amyloid-β expression and ageing, are associated with a decline in the native expression of syndapin-2 within the brain endothelium. Our data reveals that syndapin-2-mediated pathway, and its balance with the endosomal sorting, are important for amyloid-β clearance proposing a measure to evaluate Alzheimer's disease and ageing, as well as a target for counteracting amyloid-β build-up. Moreover, we provide evidence for the impact of the avidity of amyloid-β assemblies in their trafficking across the brain endothelium and in low-density lipoprotein receptor-related protein 1 expression levels, which may affect the overall clearance of amyloid-β across the blood-brain barrier.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022","modification":"2025-04-22T04:49:00.925Z","creation":"2025-04-05T21:04:02.391Z"},"accession":"S-EPMC8882007","cross_references":{"pubmed":["35233527"],"doi":["10.1093/braincomms/fcac039"]}}