TY - JOUR
T1 - Association of Head Injury with Brain Amyloid Deposition
T2 - The ARIC-PET Study
AU - Schneider, Andrea L.C.
AU - Selvin, Elizabeth
AU - Liang, Menglu
AU - Latour, Lawrence
AU - Turtzo, L. Christine
AU - Koton, Silvia
AU - Coresh, Josef
AU - Mosley, Thomas
AU - Whitlow, Christopher T.
AU - Zhou, Yun
AU - Wong, Dean Foster
AU - Ling, Geoffrey
AU - Gottesman, Rebecca F.
N1 - Funding Information:
Funding: The ARIC Study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute (NHLBI) contracts HHSN268201100005C, HHSN268201100006C, HHSN 268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN268201100011C, and HHSN26 8201100012C. Neurocognitive data are collected with funding from grants U01 HL096812, HL096814, HL096899, HL096902, and HL096917 from the National Institute of Neurological Disorders and Stroke (NINDS), with previous brain MRI examinations funded by grant R01-HL70825 from the NHLBI. The ARIC-PET study is funded by the National Institute on Aging (NIA) grant R01AG040282. Dr. Schneider is supported by the National Institutes of Health (NIH)/NINDS through an administrative supplement to award R25NS065729. Dr. Gottesman is also supported by the NIH/NIA grant K24AG052573. Dr. Selvin is supported by NIH/NIDDK grant K24DK106414. Avid Radiopharmaceuticals provided the florbetapir isotope for the study.
Publisher Copyright:
© Copyright 2019, Mary Ann Liebert, Inc., publishers 2019.
PY - 2019/9
Y1 - 2019/9
N2 - 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 department/hospitalization International Classification of Diseases, Ninth Revision 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 also was 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 with persons with a history of one 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.
AB - 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 department/hospitalization International Classification of Diseases, Ninth Revision 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 also was 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 with persons with a history of one 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.
KW - PET amyloid imaging
KW - cohort study
KW - epidemiology
KW - head injury
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U2 - 10.1089/neu.2018.6213
DO - 10.1089/neu.2018.6213
M3 - Article
C2 - 30963804
AN - SCOPUS:85071786983
VL - 36
SP - 2549
EP - 2557
JO - Central Nervous System Trauma
JF - Central Nervous System Trauma
SN - 0897-7151
IS - 17
ER -