Journal
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
Volume 77, Issue 1, Pages 50-63Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/jnen/nlx101
Keywords
alpha-Synuclein; beta-Amyloid; Hyperphosphorylated tau; Neurodegeneration; Neurofibrillary tangle; Proteinopathy; Traumatic brain injury
Categories
Funding
- Chronic Effects of Neurotrauma Consortium (DoD VA) [W81XWH-13-2-0095]
- Brain Tissue Repository (BTR) and Neuropathology Core, CNRM, USUHS [308049-4.01-60855]
- Boston University Alzheimer's disease Center [NIA P30 AG13846, 0572063345-5]
- Department of Veterans Affairs
- Worldwide Wrestling Foundation
- Andlinger Foundation
- American Academy of Neurology/American Brain Foundation
- James S. McDonnell Foundation
- National Center for Research Resources [P41RR014075, U24 RR021382]
- National Institute for Biomedical Imaging and Bioengineering [P41EB015896, R01EB006758, R01EB019956, R21EB018907]
- National Institute on Aging [AG022381, 5R01AG008122, R01 AG016495]
- National Center for Alternative Medicine [RC1 AT005728-01]
- National Institute of Neurological Disorders and Stroke [R01NS052585-01, 1R21NS072652-01, 1R01NS070963, R01NS083534, 5U01NS086625, U01NS086625, K23NS094538]
- National Institute of Child Health and Development [K01 HD074651-01A1]
- Shared Instrumentation Grants [1S10RR023401, 1S10RR019307, 1S10RR023043]
- NIH Blueprint for Neuroscience Research [5U01-MH093765]
- National Institutes of Health [1S10RR023401, 1S10RR019307, 1S10RR023043]
- VA award [IO1RX 002170]
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [U01NS086659, K23NS094538] Funding Source: NIH RePORTER
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We report the clinical, neuroimaging, and neuropathologic characteristics of 2 patients who developed early onset dementia after a moderate-severe traumatic brain injury (TBI). Neuropathological evaluation revealed abundant beta-amyloid neuritic and cored plaques, diffuse beta-amyloid plaques, and frequent hyperphosphorylated-tau neurofibrillary tangles (NFT) involving much of the cortex, including insula and mammillary bodies in both cases. Case 1 additionally showed NFTs in both the superficial and deep cortical layers, occasional perivascular and depth-of-sulci NFTs, and parietal white matter rarefaction, which corresponded with decreased parietal fiber tracts observed on ex vivo MRI. Case 2 additionally showed NFT predominance in the superficial layers of the cortex, hypothalamus and brainstem, diffuse Lewy bodies in the cortex, amygdala and brainstem, and intraneuronal TDP-43 inclusions. The neuropathologic diagnoses were atypical Alzheimer disease (AD) with features of chronic traumatic encephalopathy and white matter loss (Case 1), and atypical AD, dementia with Lewy bodies and coexistent TDP-43 pathology (Case 2). These findings support an epidemiological association between TBI and dementia and further characterize the variety of misfolded proteins that may accumulate after TBI. Analyses with comprehensive clinical, imaging, genetic, and neuropathological data are required to characterize the full clinicopathological spectrum associated with dementias occurring aftermoderate-severe TBI.
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