Repetitive head impacts (RHIs) from football are associated with the neurodegenerative tauopathy chronic traumatic encephalopathy (CTE). It is unclear whether a history of traumatic brain injury (TBI) is sufficient to precipitate CTE neuropathology. We examined the association between TBI and CTE neuropathology in 580 deceased individuals exposed to RHIs from football. TBI history was assessed using a modified version of the Ohio State University TBI Identification Method Short Form administered to informants. There were 22 donors who had no TBI, 213 who had at least one TBI without loss of consciousness (LOC), 345 who had TBI with LOC, and, of those with a history of TBI with LOC, 36 who had at least one moderate-to-severe TBI (msTBI, LOC >30 min). CTE neuropathology was diagnosed in 405. There was no association between CTE neuropathology status or severity and TBI with LOC (odds ratio [OR] = 0.95, 95% confidence interval [CI] = 0.64-1.41; OR = 1.22, 95% CI = 0.71-2.09) or msTBI (OR = 0.70, 95% CI = 0.33-1.50; OR = 1.01, 95% CI = 0.30-3.41). There were no associations with other neurodegenerative or cerebrovascular pathologies examined. TBI with LOC and msTBI were not associated with CTE neuropathology in this sample of brain donors exposed to RHIs from American football.
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http://dx.doi.org/10.1089/neu.2023.0391 | DOI Listing |
Alzheimers Dement
December 2024
Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Background: Enlarged perivascular spaces (ePVS) on MRI can signal impaired cerebral fluid clearance and predict dementia risk. Risk factors and biological correlates of ePVS are uncertain partially due to the lack of pathological correlation studies. Repetitive head impacts (RHI) from contact sports might represent one risk factor for ePVS, given their association with vascular pathologies and chronic traumatic encephalopathy (CTE), a neurodegenerative disease characterized by perivascular p-tau aggregates.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Boston University Alzheimer's Disease Research Center, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Background: Traumatic encephalopathy syndrome (TES) is the proposed clinical syndrome of the neurodegenerative disease chronic traumatic encephalopathy (CTE). As part of the 2021 TES NINDS consensus diagnostic criteria, certainty levels of underlying CTE neuropathology can be determined (i.e.
View Article and Find Full Text PDFBackground: Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy specific to individuals with repetitive head trauma. Traumatic encephalopathy syndrome (TES) is the proposed clinical syndrome resulting from CTE with or without other contributing neuropathologies. Pathophysiological mechanisms driving CTE and underlying TES symptoms are not understood.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, ON, Canada.
Background: In-vivo detection of neuropathology is critical for early diagnosis of neurodegenerative diseases. Post-mortem brain magnetic resonance imaging (MRI) of pathological protein inclusions could further our ability to detect them in vivo and correlate MRI parameters to histopathological substrates. In this post-mortem study, we aimed to identify MRI correlates of neurodegenerative disease pathology in a brain with various forms of proteinopathies.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Pathology, Molecular, and Cell-Based Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Introduction: Alzheimer's disease (AD), primary age-related tauopathy (PART), and chronic traumatic encephalopathy (CTE) all feature hyperphosphorylated tau (p-tau)-immunoreactive neurofibrillary degeneration, but differ in neuroanatomical distribution and progression of neurofibrillary degeneration and amyloid beta (Aβ) deposition.
Methods: We used Nanostring GeoMx Digital Spatial Profiling to compare the expression of 70 proteins in neurofibrillary tangle (NFT)-bearing and non-NFT-bearing neurons in hippocampal CA1, CA2, and CA4 subregions and entorhinal cortex of cases with autopsy-confirmed AD (n = 8), PART (n = 7), and CTE (n = 5).
Results: There were numerous subregion-specific differences related to Aβ processing, autophagy/proteostasis, inflammation, gliosis, oxidative stress, neuronal/synaptic integrity, and p-tau epitopes among these different disorders.
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