Chronic traumatic encephalopathy and aging-related tau astrogliopathy in community-dwelling older persons with and without moderate-to-severe traumatic brain injury

Abstract This study examined the frequency of chronic traumatic encephalopathy-neuropathologic change (CTE-NC) and aging-related tau astrogliopathy (ARTAG) in community-dwelling older adults and tested the hypothesis that these tau pathologies are associated with a history of moderate-to-severe trau...

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Published in:Journal of neuropathology and experimental neurology 2024-02, Vol.83 (3), p.181-193
Main Authors: Agrawal, Sonal, Leurgans, Sue E, Barnes, Lisa L, Dams-O’Connor, Kristen, Mez, Jesse, Bennett, David A, Schneider, Julie A
Format: Article
Language:English
Subjects:
Aged
Aged, 80 and over
Aging - pathology
Alzheimer Disease - pathology
Amyloid beta-Peptides
Astrocytes - pathology
Brain - pathology
Brain Injuries, Traumatic - complications
Brain Injuries, Traumatic - pathology
Chronic traumatic encephalopathy
Chronic Traumatic Encephalopathy - pathology
Humans
Independent Living
Older people
Original
tau Proteins - metabolism
Traumatic brain injury
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Summary:Abstract This study examined the frequency of chronic traumatic encephalopathy-neuropathologic change (CTE-NC) and aging-related tau astrogliopathy (ARTAG) in community-dwelling older adults and tested the hypothesis that these tau pathologies are associated with a history of moderate-to-severe traumatic brain injury (msTBI), defined as a TBI with loss of consciousness >30 minutes. We evaluated CTE-NC, ARTAG, and Alzheimer disease pathologies in 94 participants with msTBI and 94 participants without TBI matched by age, sex, education, and dementia status TBI from the Rush community-based cohorts. Six (3%) of brains showed the pathognomonic lesion of CTE-NC; only 3 of these had a history of msTBI. In contrast, ARTAG was common in older brains (gray matter ARTAG = 77%; white matter ARTAG = 54%; subpial ARTAG = 51%); there were no differences in severity, type, or distribution of ARTAG pathology with respect to history of msTBI. Furthermore, those with msTBI did not have higher levels of PHF-tau tangles density but had higher levels of amyloid-β load (Estimate = 0.339, SE = 0.164, p = 0.040). These findings suggest that CTE-NC is infrequent while ARTAG is common in the community and that both pathologies are unrelated to msTBI. The association of msTBI with amyloid-β, rather than with tauopathies suggests differential mechanisms of neurodegeneration in msTBI.
ISSN:0022-3069
1554-6578
DOI:10.1093/jnen/nlae007