{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kirsch D"],"funding":["National Institute of Neurological Disorders and Stroke","BLRD VA","National Institute of Aging Boston University AD Center","Andlinger Foundation","United States (U.S.) Department of Veterans Affairs, Veterans Health Administration, Clinical Sciences Research and Development Merit Award","National Institute of Aging","NIA NIH HHS","Alzheimer Association","Biomedical Laboratory Research and Development CDA2","NHLBI NIH HHS","Department of Defense Peer Reviewed Alzheimer Research Program","VA","National Heart, Lung and Blood Institute","World Wrestling Entertainment, Inc.","NINDS NIH HHS","Concussion Legacy Foundation","Alzheimer's Association"],"pagination":["127-139"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9852946"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["82(2)"],"pubmed_abstract":["Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease linked to repetitive head impacts (RHI) and characterized by perivascular hyperphosphorylated tau (p-tau) deposits. The role of vascular injury, blood-brain barrier leakage, and neuroinflammation in CTE pathogenesis is not well understood. We performed quantitative immunoassays for intercellular adhesion molecule 1 (ICAM1), vascular cellular adhesion molecule 1 (VCAM1), and C-reactive protein (CRP) within the postmortem dorsolateral frontal cortex of participants with and without a history of RHI and CTE (n = 156), and tested for associations with RHI, microgliosis, and tau pathology measures. Levels of vascular injury-associated markers ICAM1, VCAM1, and CRP were increased in CTE compared to RHI-exposed and -naïve controls. ICAM1 and CRP increased with RHI exposure duration (p < 0.01) and were associated with increased microglial density (p < 0.001) and tau pathology (AT8, p-tau396, p-tau202; p < 0.05). Histologically, there was significantly increased ICAM1 staining of the microvasculature, extracellular space, and astrocytes at the sulcal depths in high stage CTE compared to both low stage CTE and controls. Multifocal perivascular immunoreactivity for serum albumin was present in all RHI-exposed individuals. These findings demonstrate that vascular injury markers are associated with RHI exposure, duration, and microgliosis, are elevated in CTE, and increase with disease severity."],"journal":["Journal of neuropathology and experimental neurology"],"pubmed_title":["Vascular injury is associated with repetitive head impacts and tau pathology in chronic traumatic encephalopathy."],"pmcid":["PMC9852946"],"funding_grant_id":["PRARP #13267017","U54NS115266","I01BX005933","NIRG-362697","RF1 NS122854","I01 BX005933","IK2 BX004349","F31NS127449","HHSN2682015000011","75N92019D00031","U54 NS115266","I01BX005161","P30 AG072978","U19 AG068753","HHSN268201500011C","5IK2BX004349","HHSN268201500001C","U01NS086659","NIRG-305779","R01 AG075876","U01 NS086659","RF1NS122854","R01AG075876","HHSN268201000011C","U19AG068753","F31 NS127449","HHSN268201500001I","I01 BX005161","P30AG072978"],"pubmed_authors":["Mathias R","Huber BR","Alvarez VE","Aytan N","Kelley H","Xia W","Stein TD","McKee AC","Kubilus C","Cormier K","Shah A","Dixon E","Daley S","Kirsch D","Cherry JD"],"additional_accession":[]},"is_claimable":false,"name":"Vascular injury is associated with repetitive head impacts and tau pathology in chronic traumatic encephalopathy.","description":"Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease linked to repetitive head impacts (RHI) and characterized by perivascular hyperphosphorylated tau (p-tau) deposits. The role of vascular injury, blood-brain barrier leakage, and neuroinflammation in CTE pathogenesis is not well understood. We performed quantitative immunoassays for intercellular adhesion molecule 1 (ICAM1), vascular cellular adhesion molecule 1 (VCAM1), and C-reactive protein (CRP) within the postmortem dorsolateral frontal cortex of participants with and without a history of RHI and CTE (n = 156), and tested for associations with RHI, microgliosis, and tau pathology measures. Levels of vascular injury-associated markers ICAM1, VCAM1, and CRP were increased in CTE compared to RHI-exposed and -naïve controls. ICAM1 and CRP increased with RHI exposure duration (p < 0.01) and were associated with increased microglial density (p < 0.001) and tau pathology (AT8, p-tau396, p-tau202; p < 0.05). Histologically, there was significantly increased ICAM1 staining of the microvasculature, extracellular space, and astrocytes at the sulcal depths in high stage CTE compared to both low stage CTE and controls. Multifocal perivascular immunoreactivity for serum albumin was present in all RHI-exposed individuals. These findings demonstrate that vascular injury markers are associated with RHI exposure, duration, and microgliosis, are elevated in CTE, and increase with disease severity.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2026-04-08T12:11:16.909Z","creation":"2025-02-19T02:23:58.78Z"},"accession":"S-EPMC9852946","cross_references":{"pubmed":["36617181"],"doi":["10.1093/jnen/nlac122"]}}