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

J Neuropathol Exp Neurol. 2024 Feb 21;83(3):181-193. doi: 10.1093/jnen/nlae007.


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.

Keywords: ARTAG; Amyloid-β; CTE; Community-based study; Tau; Traumatic brain injury.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • 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* / pathology
  • Humans
  • Independent Living
  • tau Proteins / metabolism


  • tau Proteins
  • Amyloid beta-Peptides