{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["DiBona VL"],"funding":["US Department of Defense Military Health System","NIMH NIH HHS","New Jersey Commission on Brain Injury Research","NINDS NIH HHS","National Institutes of Health","NIGMS NIH HHS"],"pagination":["99-109"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8449802"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["172"],"pubmed_abstract":["Within the brain, traumatic brain injury (TBI) alters synaptic plasticity and increases neuroinflammation and neuronal death. Yet, there lacks effective TBI treatments providing pleiotropic beneficial effects on these diverse cellular processes necessary for functional recovery. Here, we show the diabetes drug, metformin, significantly improves cognitive functions after controlled cortical impact (CCI) injury in mice, showing improved spatial learning and nest building. Furthermore, injured animals treated with metformin exhibit increased ramification of microglia processes, indicating reduced neuroinflammation. Finally, metformin treatment in vitro increased neuronal activation of partitioning defective 1 (Par1), a family of Ser/Thr kinases playing a key role in synaptic plasticity and neuroinflammation. These results suggest metformin is a promising therapeutic agent for targeting multiple cellular processes necessary for functional TBI recovery."],"journal":["Neuroscience research"],"pubmed_title":["Metformin reduces neuroinflammation and improves cognitive functions after traumatic brain injury."],"pmcid":["PMC8449802"],"funding_grant_id":["R25 MH095722","R00 NS065183","K12 GM093854","R01 NS089578"],"pubmed_authors":["Shah MK","Crockett DP","Zhang H","DiBona VL","Krause KJ","Zhu W","Voglewede MM","Smith DM"],"additional_accession":[]},"is_claimable":false,"name":"Metformin reduces neuroinflammation and improves cognitive functions after traumatic brain injury.","description":"Within the brain, traumatic brain injury (TBI) alters synaptic plasticity and increases neuroinflammation and neuronal death. Yet, there lacks effective TBI treatments providing pleiotropic beneficial effects on these diverse cellular processes necessary for functional recovery. Here, we show the diabetes drug, metformin, significantly improves cognitive functions after controlled cortical impact (CCI) injury in mice, showing improved spatial learning and nest building. Furthermore, injured animals treated with metformin exhibit increased ramification of microglia processes, indicating reduced neuroinflammation. Finally, metformin treatment in vitro increased neuronal activation of partitioning defective 1 (Par1), a family of Ser/Thr kinases playing a key role in synaptic plasticity and neuroinflammation. These results suggest metformin is a promising therapeutic agent for targeting multiple cellular processes necessary for functional TBI recovery.","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Nov","modification":"2025-04-05T13:42:44.975Z","creation":"2025-04-05T13:42:44.975Z"},"accession":"S-EPMC8449802","cross_references":{"pubmed":["34023358"],"doi":["10.1016/j.neures.2021.05.007"]}}