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.

Funder

NIH

Publisher

Oxford University Press (OUP)

Subject

Cellular and Molecular Neuroscience,Neurology (clinical),Neurology,General Medicine,Pathology and Forensic Medicine

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