{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cho FS"],"funding":["NCRR NIH HHS","NIMH NIH HHS","NINDS NIH HHS","NCI NIH HHS"],"pagination":["eabj4310"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9491689"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(652)"],"pubmed_abstract":["Inflammatory processes induced by brain injury are important for recovery; however, when uncontrolled, inflammation can be deleterious, likely explaining why most anti-inflammatory treatments have failed to improve neurological outcomes after brain injury in clinical trials. In the thalamus, chronic activation of glial cells, a proxy of inflammation, has been suggested as an indicator of increased seizure risk and cognitive deficits that develop after cortical injury. Furthermore, lesions in the thalamus, more than other brain regions, have been reported in patients with viral infections associated with neurological deficits, such as SARS-CoV-2. However, the extent to which thalamic inflammation is a driver or by-product of neurological deficits remains unknown. Here, we found that thalami"],"journal":["Science translational medicine"],"pubmed_title":["Enhancing GAT-3 in thalamic astrocytes promotes resilience to brain injury in rodents."],"pmcid":["PMC9491689"],"funding_grant_id":["R35 NS111583","R01 NS096369","P30 CA082103","F31 NS111819","DP2 MH116507","R01 NS121287","R00 NS078118","DP1 MH104069","R01 MH119349","C06 RR018928"],"pubmed_authors":["Cho FS","Anink JJ","Molofsky AV","Khakh BS","van Vliet EA","Morningstar AR","Ciesielska A","Broekaart DWM","Voskobiynyk Y","Paz JT","Vainchtein ID","Higashikubo B","Aparicio F","Aronica E","Yu X"],"additional_accession":[]},"is_claimable":false,"name":"Enhancing GAT-3 in thalamic astrocytes promotes resilience to brain injury in rodents.","description":"Inflammatory processes induced by brain injury are important for recovery; however, when uncontrolled, inflammation can be deleterious, likely explaining why most anti-inflammatory treatments have failed to improve neurological outcomes after brain injury in clinical trials. In the thalamus, chronic activation of glial cells, a proxy of inflammation, has been suggested as an indicator of increased seizure risk and cognitive deficits that develop after cortical injury. Furthermore, lesions in the thalamus, more than other brain regions, have been reported in patients with viral infections associated with neurological deficits, such as SARS-CoV-2. However, the extent to which thalamic inflammation is a driver or by-product of neurological deficits remains unknown. Here, we found that thalami","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jul","modification":"2025-04-04T23:14:30.718Z","creation":"2024-11-09T20:49:45.781Z"},"accession":"S-EPMC9491689","cross_references":{"pubmed":["35857628"],"doi":["10.1126/scitranslmed.abj4310"]}}