{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Bhatt S"],"funding":["NCATS NIH HHS","VA National Center for PTSD","Gustavus and Louise Pfeiffer Research Foundation","NIMH NIH HHS","NIAAA NIH HHS","U.S. Department of Health &amp; Human Services | NIH | National Institute of Mental Health","NIGMS NIH HHS"],"pagination":["2360"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7217830"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(1)"],"pubmed_abstract":["Despite well-known peripheral immune activation in posttraumatic stress disorder (PTSD), there are no studies of brain immunologic regulation in individuals with PTSD. [<sup>11</sup>C]PBR28 Positron Emission Tomography brain imaging of the 18-kDa translocator protein (TSPO), a microglial biomarker, was conducted in 23 individuals with PTSD and 26 healthy individuals-with or without trauma exposure. Prefrontal-limbic TSPO availability in the PTSD group was negatively associated with PTSD symptom severity and was significantly lower than in controls. Higher C-reactive protein levels were also associated with lower prefrontal-limbic TSPO availability and PTSD severity. An independent postmortem study found no differential gene expression in 22 PTSD vs. 22 controls, but showed lower relative expression of TSPO and microglia-associated genes TNFRSF14 and TSPOAP1 in a female PTSD subgroup. These findings suggest that peripheral immune activation in PTSD is associated with deficient brain microglial activation, challenging prevailing hypotheses positing neuroimmune activation as central to stress-related pathophysiology."],"journal":["Nature communications"],"pubmed_title":["PTSD is associated with neuroimmune suppression: evidence from PET imaging and postmortem transcriptomic studies."],"pmcid":["PMC7217830"],"funding_grant_id":["R01MH110674","K01 AA024788","F30 MH116607","F30MH116607","T32 GM007205","UL1 TR001863","R01 MH110674"],"pubmed_authors":["Davis MT","Friedman MJ","Traumatic Stress Brain Study Group","Pietrzak RH","Hillmer AT","Rusowicz A","Duman RS","Bhatt S","Matuskey D","Angarita GA","Krystal JH","Girgenti MJ","Huang Y","Southwick SM","Kapinos M","Nabulsi N","Carson RE","Esterlis I","Cosgrove KP"],"additional_accession":[]},"is_claimable":false,"name":"PTSD is associated with neuroimmune suppression: evidence from PET imaging and postmortem transcriptomic studies.","description":"Despite well-known peripheral immune activation in posttraumatic stress disorder (PTSD), there are no studies of brain immunologic regulation in individuals with PTSD. [<sup>11</sup>C]PBR28 Positron Emission Tomography brain imaging of the 18-kDa translocator protein (TSPO), a microglial biomarker, was conducted in 23 individuals with PTSD and 26 healthy individuals-with or without trauma exposure. Prefrontal-limbic TSPO availability in the PTSD group was negatively associated with PTSD symptom severity and was significantly lower than in controls. Higher C-reactive protein levels were also associated with lower prefrontal-limbic TSPO availability and PTSD severity. An independent postmortem study found no differential gene expression in 22 PTSD vs. 22 controls, but showed lower relative expression of TSPO and microglia-associated genes TNFRSF14 and TSPOAP1 in a female PTSD subgroup. These findings suggest that peripheral immune activation in PTSD is associated with deficient brain microglial activation, challenging prevailing hypotheses positing neuroimmune activation as central to stress-related pathophysiology.","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 May","modification":"2026-05-02T00:19:03.557Z","creation":"2020-05-22T20:19:52Z"},"accession":"S-EPMC7217830","cross_references":{"pubmed":["32398677"],"doi":["10.1038/s41467-020-15930-5"]}}