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Traumatic brain injury and Alzheimer's disease neuropathology
Author(s) -
Jellinger Kurt A.
Publication year - 2019
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2019.06.3917
Subject(s) - neuropathology , citation , psychoanalysis , psychology , library science , medicine , disease , computer science , pathology
Sir, Traumatic brain injury (TBI) as a risk factor for the development of late-life dementia, including Alzheimer’s disease (AD), is a matter of discussion [1–4], and only a few studies examined the potential relationship between residual TBI lesions and AD neuropathology [5–9]. Examining 4761 deceased participants from the National Alzheimer’s Coordination Center (NACC) of the years 2005 to 2017, Sugarman et al. [8] reported that among 453 cases with self-reported TBI with loss of consciousness (mean age: 77.76 12.3 years), 250 (73.1%) showed definite AD pathology (defined by the Consortium to Establish a Registry for Alzheimer’s Disease [CERAD] scores 2 or 3 and Braak scores 3), whereas among 4208 cases (mean age: 80.36 10.9 years; P, .01) without a history of remote TBI, 2572 (74.0%) were definite AD. These data indicated that self-reported TBI with loss of consciousness may not be an independent risk for clinical and pathological AD. They are in accordance with two clinicopathological studies showing that remote TBI may not increase the risk of AD [3,9]. Following previous studies on the incidence of AD pathology after blunt TBI and the frequency of TBI residuals in autopsy cases with and without definite AD [5], we examined 1677 autopsy cases from two large hospital centers in Vienna, Austria, between 1985 and 2009. The results were as follows: 1. Among 186 autopsy cases (mean age: 70.16 12.8 years) with residuals of blunt TBI (old concussion defects mainly in the frontobasal, frontopolar, polar, or temporopolar regions), 26 cases (13.9%; mean age: 77 6 10.7 years) revealed the pathological features of definite AD (CERAD score B or C, Braak score 4-5 to 6). APOE carriers were ε3/ε3 (n 5 20), ε3/ε4 (n 5 3), ε2/ε3 (n 5 3), and ε2/ε2 (n 5 1). The history of TBI dated between one and 30 years; the duration of AD ranged from3 to7years.Among1115 controls (CERAD score 0-A,Braak score, 4,mean age: 77.36 9.4 years), 159 cases or 14.1% (mean age: 68.9 6 10.7 years)