{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ojelade SA"],"funding":["NICHD NIH HHS","NIA NIH HHS","Howard Hughes Medical Institute","NCRR NIH HHS","Burroughs Wellcome Fund","NINDS NIH HHS","NCI NIH HHS","American Federation for Aging Research","National Institutes of Health","Alzheimer's Association","NIGMS NIH HHS"],"pagination":["1799-1813.e5"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6703184"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["28(7)"],"pubmed_abstract":["The Alzheimer's disease (AD) susceptibility gene, CD2-associated protein (CD2AP), encodes an actin binding adaptor protein, but its function in the nervous system is largely unknown. Loss of the Drosophila ortholog cindr enhances neurotoxicity of human Tau, which forms neurofibrillary tangle pathology in AD. We show that Cindr is expressed in neurons and present at synaptic terminals. cindr mutants show impairments in synapse maturation and both synaptic vesicle recycling and release. Cindr associates and genetically interacts with 14-3-3ζ, regulates the ubiquitin-proteasome system, and affects turnover of Synapsin and the plasma membrane calcium ATPase (PMCA). Loss of cindr elevates PMCA levels and reduces cytosolic calcium. Studies of Cd2ap null mice support a conserved role in synaptic "],"journal":["Cell reports"],"pubmed_title":["cindr, the Drosophila Homolog of the CD2AP Alzheimer's Disease Risk Gene, Is Required for Synaptic Transmission and Proteostasis."],"pmcid":["PMC6703184"],"funding_grant_id":["R01 AG015819","U01 AG061357","R01 AG057339","R01 AG054076","R01 AG036836","P30 AG066546","P30 AG010161","R01 AG050631","R01 NS017950","U01 AG052409","P30 CA125123","R01 AG053960","R01 AG036042","U01 AG046152","R01 AG033193","RC2 AG036547","U01 AG046161","C06 RR029965","R01 GM120033","U54 HD083092","R01 AG017917","P30 AG010129"],"pubmed_authors":["Yu L","Ojelade SA","Petyuk V","Zuo Z","Shulman JM","Giagtzoglou N","Li Y","Duraine L","Bennett DA","Lee TV","Arenkiel BR","Ugur B","De Jager PL","Bellen HJ"],"additional_accession":[]},"is_claimable":false,"name":"cindr, the Drosophila Homolog of the CD2AP Alzheimer's Disease Risk Gene, Is Required for Synaptic Transmission and Proteostasis.","description":"The Alzheimer's disease (AD) susceptibility gene, CD2-associated protein (CD2AP), encodes an actin binding adaptor protein, but its function in the nervous system is largely unknown. Loss of the Drosophila ortholog cindr enhances neurotoxicity of human Tau, which forms neurofibrillary tangle pathology in AD. We show that Cindr is expressed in neurons and present at synaptic terminals. cindr mutants show impairments in synapse maturation and both synaptic vesicle recycling and release. Cindr associates and genetically interacts with 14-3-3ζ, regulates the ubiquitin-proteasome system, and affects turnover of Synapsin and the plasma membrane calcium ATPase (PMCA). Loss of cindr elevates PMCA levels and reduces cytosolic calcium. Studies of Cd2ap null mice support a conserved role in synaptic ","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Aug","modification":"2025-04-29T10:46:16.96Z","creation":"2019-08-26T07:04:10Z"},"accession":"S-EPMC6703184","cross_references":{"pubmed":["31412248"],"doi":["10.1016/j.celrep.2019.07.041"]}}