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

Author:

Agrawal Sonal12ORCID,Leurgans Sue E13,Barnes Lisa L134,Dams-O’Connor Kristen56,Mez Jesse78,Bennett David A13,Schneider Julie A123

Affiliation:

1. Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, Illinois, USA

2. Department of Pathology, Rush University Medical Center, Chicago, Illinois, USA

3. Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA

4. Department of Behavioral Sciences, Rush University Medical Center, Chicago, Illinois, USA

5. Department of Rehabilitation and Human Performance, Mt Sinai School of Medicine, New York, New York, USA

6. Department of Neurology, Mt Sinai School of Medicine, New York, New York, USA

7. Boston University Alzheimer’s Disease Research Center, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, USA

8. Boston University Chronic Traumatic Encephalopathy Center, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, USA

Abstract

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.

Publisher

Oxford University Press (OUP)

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