{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhou Y"],"funding":["Natural Science Foundation of Hubei Province","National Key R&D Program of China","National Natural Science Foundation of China","Hubei Provincial Natural Science Foundation","National Key Research and Development Program of China","Science and Technology Innovation Program of Hunan Province"],"pagination":["e02535"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12499468"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(37)"],"pubmed_abstract":["Diabetic encephalopathy (DE) is a severe complication of diabetes characterized by cognitive impairment and synaptic dysfunction, while the underlying mechanisms are not clear. Here, a critical role is identified for death-associated protein kinase 1 (DAPK1) in DE pathogenesis using transgenic and streptozotocin-induced diabetic mouse models. Elevated DAPK1 expression in hippocampal excitatory neurons correlates with cognitive deficits, increases neuronal apoptosis, and disrupts synaptic plasticity. Conditional knockout of DAPK1 in CaMKII-positive neurons significantly mitigates these pathological features, improving cognitive performance and synaptic function. Mechanistically, it is demonstrated that reduced hippocampal microRNA (miR)-216a-5p levels in diabetic mice lead to DAPK1 upregula"],"journal":["Advanced science (Weinheim, Baden-Wurttemberg, Germany)"],"pubmed_title":["Epigenetic Regulation of DAPK1 and Netrin-1 Drives Diabetic Encephalopathy."],"pmcid":["PMC12499468"],"funding_grant_id":["2022ZD0211800","82325017","2024JJ7442","82261138555","2022CFA004","82401423","82371403","82030032","2023AFA068","2022RC4044"],"pubmed_authors":["Fan HW","Li WL","Shu K","Liu LJ","Zhou Y","Kou JX","Zheng K","Hu F","Chu LL","Guo ZX","Yin JW","Brazhe N","Liu D","Xiang ZG","Zhu LQ"],"additional_accession":[]},"is_claimable":false,"name":"Epigenetic Regulation of DAPK1 and Netrin-1 Drives Diabetic Encephalopathy.","description":"Diabetic encephalopathy (DE) is a severe complication of diabetes characterized by cognitive impairment and synaptic dysfunction, while the underlying mechanisms are not clear. Here, a critical role is identified for death-associated protein kinase 1 (DAPK1) in DE pathogenesis using transgenic and streptozotocin-induced diabetic mouse models. Elevated DAPK1 expression in hippocampal excitatory neurons correlates with cognitive deficits, increases neuronal apoptosis, and disrupts synaptic plasticity. Conditional knockout of DAPK1 in CaMKII-positive neurons significantly mitigates these pathological features, improving cognitive performance and synaptic function. Mechanistically, it is demonstrated that reduced hippocampal microRNA (miR)-216a-5p levels in diabetic mice lead to DAPK1 upregula","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Oct","modification":"2026-06-04T04:47:24.505Z","creation":"2026-05-05T03:12:29.306Z"},"accession":"S-EPMC12499468","cross_references":{"pubmed":["40787892"],"doi":["10.1002/advs.202502535"]}}