Association of Traumatic Brain Injury With and Without Loss of Consciousness With Neuropathologic Outcomes in Community-Dwelling Older Persons.
Association of Traumatic Brain Injury With and Without Loss of Consciousness With Neuropathologic Outcomes in Community-Dwelling Older Persons.
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DOI：
10.1001/jamanetworkopen.2022.9311
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发表时间：
2022-04-01
影响因子：
13.8
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中科院分区：
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伴或不伴意识丧失的创伤性脑损伤与老年人痴呆相关的神经病理学结果相关吗？在这项对来自3项社区队列研究的1689例尸检参与者的横断面分析中，TBI伴发脑梗死的参与者有更大的淀粉样蛋白-β负荷和更高的总梗死和微梗死几率，而TBI不伴发脑梗死的参与者有更高的新皮质路易体和皮质微梗死几率。即使没有脑外伤，TBI也可能与以后生活中神经退行性和血管病理学发现的更高几率相关。这项对尸检参与者的横断面研究评估了伴有和不伴有意识丧失的创伤性脑损伤（TBI）是否与老年人痴呆相关的神经病理学结局相关。创伤性脑损伤（TBI）史被认为是阿尔茨海默氏痴呆症的危险因素。然而，TBI的具体关联，即使没有意识丧失（意识丧失），与阿尔茨海默氏症的病理结果，包括阿尔茨海默病（AD），非AD神经退行性，血管病理结果，仍然不清楚。在社区人群中研究TBI伴或不伴脑梗死与神经病理学结果之间的关系。这项横断面分析使用了来自宗教秩序研究、拉什记忆和衰老项目以及少数民族衰老研究的1689名参与者的神经病理学数据。这些研究分别于1994年、1997年和2004年开始招募。当前研究的数据集于2021年4月3日冻结，当时参与者的平均（SD）随访时间为8.7（5.5）年。在基线和年度随访时，使用标准化的自我报告问卷评估创伤性脑损伤暴露。参与者被分为（1）没有TBI暴露（n = 1024），（2）TBI伴TBI（n = 161），或（3）TBI不伴TBI（n = 504）。评估了β淀粉样蛋白、成对螺旋丝缠结、新皮质路易体、反式反应DNA结合蛋白43、海马硬化、大体梗死和微梗死的神经病理学指标。多元线性回归和逻辑回归模型被用来确定是否TBI与或不TBI暴露（与没有TBI暴露作为参考组）与神经病理结果调整后的死亡年龄，性别和教育水平。载脂蛋白E（APOE）ε4等位基因和性别差异是否改变了相关性也进行了检查。共有1689名受试者（1138名[67%]女性和551名[33%]男性;平均[SD]死亡年龄为89.2 [6.7]岁; 80名[5%]黑人、46名[3%]拉丁裔、1639名[97%]非拉丁裔和1601名[95%]白色）参加了本研究。与没有TBI的参与者相比，TBI合并TBI的参与者有更大的β淀粉样蛋白负荷（估计值，0.25; 95% CI，0.06-0.43; P = 0.008）和发生1次或多次大体梗死的几率更高（比值比[OR]，1.45; 95% CI，1.04-2.02; P = .02）和1个或多个微梗死（OR，1.70; 95% CI，1.21-2.38; P = .002），尤其是皮质下微梗死（OR，1.85; 95% CI，1.23-2.79; P = .002）。无脑梗死的TBI患者出现新皮质路易体（OR，1.37; 95%CI，1.01-1.87; P = .04）和1个或多个皮质微梗死（OR，1.43; 95%CI，1.09-1.87; P = .008）的几率较高。在控制了血管危险因素和血管疾病负担后，TBI伴或不伴血管病变与血管病理结果的相关性仍然存在。创伤性脑损伤伴或不伴海马硬化与成对螺旋丝缠结、反式反应DNA结合蛋白43或海马硬化无关。与APOE ε4或性别无相互作用。这种横断面分析表明，TBI史，即使没有脑外伤，与年龄相关的神经病理结果，神经退行性和血管。神经病理学结果的变化，在个人和没有脑外伤可能提供线索的潜在机制，诊断和管理的人与TBI。
Is traumatic brain injury (TBI) with and without loss of consciousness (LOC) associated with dementia-related neuropathologic outcomes in older persons? In this cross-sectional analysis of 1689 autopsied participants from 3 community-based cohort studies, participants with TBI with LOC had greater amyloid-β burden and higher odds of gross infarcts and microinfarcts, whereas those with TBI without LOC had higher odds of neocortical Lewy bodies and cortical microinfarcts. Even without LOC, TBI may be associated with higher odds of neurodegenerative and vascular pathologic findings in later life. This cross-sectional study of autopsied participants assesses whether traumatic brain injury (TBI) with and without loss of consciousness is associated with dementia-related neuropathologic outcomes in older persons. A history of traumatic brain injury (TBI) has been considered a risk factor for Alzheimer dementia. However, the specific association of TBI, even without loss of consciousness (LOC), with pathologic findings that underlie Alzheimer dementia, including Alzheimer disease (AD), non-AD neurodegenerative, and vascular pathologic findings, remains unclear. To examine the association between TBI with and without LOC and neuropathologic findings in community-based cohorts. This cross-sectional analysis used neuropathologic data from 1689 participants from the Religious Orders Study, the Rush Memory and Aging Project, and the Minority Aging Research Study. These studies began enrollment in 1994, 1997, and 2004, respectively. The current study’s data set was frozen on April 3, 2021, when the mean (SD) length of follow-up for the participants was 8.7 (5.5) years. Traumatic brain injury exposure was assessed using a standardized, self-reported questionnaire at baseline and annual follow-up visits. Participants were categorized into those (1) without TBI exposure (n = 1024), (2) with TBI with LOC (n = 161), or (3) with TBI without LOC (n = 504). Neuropathologic measures of amyloid-β, paired helical filament tangles, neocortical Lewy bodies, transactive response DNA-binding protein 43, hippocampal sclerosis, gross infarcts, and microinfarcts were assessed. Multiple linear regression and logistic regression models were used to determine whether TBI with or without LOC (compared with no TBI exposure as the reference group) was associated with neuropathologic outcomes after adjusting for age at death, sex, and educational level. Whether the apolipoprotein E (APOE) ε4 allele and sex differences modified associations was also examined. A total of 1689 participants (1138 [67%] women and 551 [33%] men; mean [SD] age at death, 89.2 [6.7] years; 80 [5%] Black, 46 [3%] Latino, 1639 [97%] non-Latino, and 1601 [95%] White) participated in the study. Compared with participants without TBI, participants with TBI with LOC had a greater amyloid-β load (estimate, 0.25; 95% CI, 0.06-0.43; P = .008) and higher odds of having 1 or more gross infarcts (odds ratio [OR], 1.45; 95% CI, 1.04-2.02; P = .02) and 1 or more microinfarcts (OR, 1.70; 95% CI, 1.21-2.38; P = .002), particularly subcortical microinfarcts (OR, 1.85; 95% CI, 1.23-2.79; P = .002). Those with TBI without LOC had higher odds of neocortical Lewy bodies (OR, 1.37; 95% CI, 1.01-1.87; P = .04) and 1 or more cortical microinfarcts (OR, 1.43; 95% CI, 1.09-1.87; P = .008). The association of TBI with and without LOC with vascular pathologic outcomes persisted after controlling for vascular risk factors and vascular disease burden. Traumatic brain injury with or without LOC was not associated with paired helical filament tangles, transactive response DNA-binding protein 43, or hippocampal sclerosis. No interactions occurred with APOE ε4 or sex. This cross-sectional analysis suggests that a history of TBI, even without LOC, is associated with age-related neuropathologic outcomes, both neurodegenerative and vascular. The variation in the neuropathologic outcomes in individuals with and without LOC may provide clues to potential mechanisms, diagnoses, and management in persons with TBI.
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DOI：
10.1080/13854046.2016.1257069
发表时间：
2017-01
期刊：
The Clinical neuropsychologist
影响因子：
--
作者：
LoBue C;Wadsworth H;Wilmoth K;Clem M;Hart J Jr;Womack KB;Didehbani N;Lacritz LH;Rossetti HC;Cullum CM
通讯作者：
Cullum CM
DOI：
10.3233/jad-179939
发表时间：
2018
期刊：
Journal of Alzheimer's disease : JAD
影响因子：
--
作者：
Bennett DA;Buchman AS;Boyle PA;Barnes LL;Wilson RS;Schneider JA
通讯作者：
Schneider JA
影响因子：
14.5
作者：
Hayes, Jasmeet P.;Logue, Mark W.;Miller, Mark W.
通讯作者：
Miller, Mark W.
影响因子：
11.2
作者：
Mez, Jesse;Daneshvar, Daniel H.;McKee, Ann C.
通讯作者：
McKee, Ann C.
影响因子：
2.4
作者：
Abner, Erin L.;Nelson, Peter T.;Kryscio, Richard J.
通讯作者：
Kryscio, Richard J.