
@article{ref1,
title="Association of head injury with brain amyloid deposition: the ARIC-PET Study",
journal="Journal of neurotrauma",
year="2019",
author="Schneider, Andrea Lauren Christman and Selvin, Elizabeth and Liang, Menglu and Latour, Lawrence and Turtzo, L. Christine and Koton, Silvia and Coresh, Josef and Mosley, Thomas and Whitlow, Christopher T. and Zhou, Yun and Wong, Dean and Ling, Geoffrey and Gottesman, Rebecca F.",
volume="ePub",
number="ePub",
pages="ePub-ePub",
abstract="Our objective was to examine associations of head injury with total and regional brain amyloid deposition. We performed cross-sectional analyses of 329 non-demented participants (81 with prior head injury) in the Atherosclerosis Risk in Communities-Positron Emission Tomography (ARIC-PET) Study who underwent 18-Florbetapir PET imaging in 2012-2014. A history of head injury was defined by self-report or emergency room/hospitalization ICD-9 codes. Generalized linear regression models adjusted for demographic, socioeconomic, and dementia/cardiovascular risk factors were used to estimate prevalence ratios (PRs) (95% confidence intervals [CIs]) for elevated (>1.2) global and regional standard uptake value ratios (SUVRs). Mean age of participants was 76 years, 57% were women, and 43% were black. Head injury was associated with increased prevalence of elevated SUVR >1.2 globally (PR: 1.31, 95% CI: 1.19-1.57), as well as in the orbitofrontal cortex (PR: 1.23, 95% CI: 1.04-1.46), prefrontal cortex (PR: 1.18, 95% CI: 1.00-1.39), superior frontal cortex (PR: 1.24, 95% CI: 1.05-1.48), and posterior cingulate (PR: 1.26, 95% CI: 1.04-1.52). There was also evidence for a dose-response relationship, whereby a history of 1 head injury was associated with elevated SUVR >1.2 in the prefrontal cortex and superior frontal cortex compared to persons with a history of 1 head injury (all p<0.05). In conclusion, head injury was associated with increased amyloid deposition globally and in the frontal cortex and posterior cingulate, with suggestion of a dose-response association of head injuries with beta-amyloid deposition. Further work is needed to determine if increased amyloid deposition contributes to dementia in this population.<p /> <p>Language: en</p>",
language="en",
issn="0897-7151",
doi="10.1089/neu.2018.6213",
url="http://dx.doi.org/10.1089/neu.2018.6213"
}