创伤性脑损伤和阿尔茨海默病遗传风险对越战老兵脑脊液 β 淀粉样蛋白水平的影响。

IF 1.8 Q3 CLINICAL NEUROLOGY
Neurotrauma reports Pub Date : 2024-08-22 eCollection Date: 2024-01-01 DOI:10.1089/neur.2024.0048
Jena N Moody, Erica Howard, Kate E Nolan, Sarah Prieto, Mark W Logue, Jasmeet P Hayes
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引用次数: 0

摘要

创伤性脑损伤(TBI)可能会增加阿尔茨海默病(AD)及其神经病理学相关疾病的发病风险,但这种关系的机制尚不清楚。本研究探讨了创伤性脑损伤和阿尔茨海默病遗传风险对越战退伍军人体内β淀粉样蛋白(Aβ)水平的协同作用。我们假设,TBI 和较高的 AD 多基因风险评分 (PRS) 将与较低的脑脊液 (CSF) Aβ42/40 相关联。数据来自美国国防部阿尔茨海默病神经影像计划。参与者包括没有痴呆症的越战退伍军人,他们被认定为非西班牙裔/拉美裔白人,并拥有可用的人口统计学、临床评估、遗传学和脑脊液生物标记物数据。采用俄亥俄州立大学 TBI 鉴定方法对终生 TBI 史进行评估。参与者被分为有 TBI 史和无 TBI 史两类。在有过创伤性脑损伤的参与者中,损伤严重程度被定义为轻度或中度/重度。计算脑脊液 Aβ42/40 比率。使用PRSs评估AD的遗传倾向。层次线性回归模型检验了创伤性脑损伤和 AD PRS 对 Aβ42/40 的交互影响。探索性分析检验了 TBI 严重程度与 PRS 之间的交互作用。最终样本包括 88 名男性越战退伍军人,他们被认定为非西班牙裔/拉美裔白人(平均年龄 = 68.3 岁),其中 49 人报告曾有过创伤性脑损伤。创伤性脑损伤与 PRS 之间存在明显的交互作用,即创伤性脑损伤和 AD PRS 较高的个体的 Aβ42/40 值较低 (B = -0.45, 95% CI: -0.86 to -0.05, p = 0.03)。这种关系可能随着创伤性脑损伤严重程度的增加而增强(p = 0.05)。总体而言,创伤性脑损伤与较低的 Aβ42/40相关,表明在多基因AD风险增加的背景下,大脑中的淀粉样蛋白沉积增加。这些发现突显了哪些人在受到创伤性脑损伤后可能会增加罹患注意力缺失症神经病理学的风险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Traumatic Brain Injury and Genetic Risk for Alzheimer's Disease Impact Cerebrospinal Fluid β-Amyloid Levels in Vietnam War Veterans.

Traumatic brain injuries (TBIs) may increase the risk for Alzheimer's disease (AD) and its neuropathological correlates, although the mechanisms of this relationship are unclear. The current study examined the synergistic effects of TBI and genetic risk for AD on β-amyloid (Aβ) levels among Vietnam War Veterans. We hypothesized that the combination of TBI and higher polygenic risk score (PRS) for AD would be associated with lower cerebrospinal fluid (CSF) Aβ42/40. Data were obtained from the Department of Defense Alzheimer's Disease Neuroimaging Initiative. Participants included Vietnam War Veterans without dementia who identified as White non-Hispanic/Latino and had available demographic, clinical assessment, genetic, and CSF biomarker data. Lifetime TBI history was assessed using The Ohio State University TBI Identification Method. Participants were categorized into those with and without TBI. Among those with a prior TBI, injury severity was defined as either mild or moderate/severe. CSF Aβ42/40 ratios were calculated. Genetic propensity for AD was assessed using PRSs. Hierarchical linear regression models examined the interactive effects of TBI and PRS for AD on Aβ42/40. Exploratory analyses examined the interaction between TBI severity and PRS. The final sample included 88 male Vietnam War Veterans who identified as White non-Hispanic/Latino (M age = 68.3 years), 49 of whom reported a prior TBI. There was a significant interaction between TBI and PRS, such that individuals with TBI and higher PRS for AD had lower Aβ42/40 (B = -0.45, 95% CI: -0.86 to -0.05, p = 0.03). This relationship may be stronger with increasing TBI severity (p = 0.05). Overall, TBI was associated with lower Aβ42/40, indicating greater amyloid deposition in the brain, in the context of greater polygenic risk for AD. These findings highlight who may be at increased risk for AD neuropathology following TBI.

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CiteScore
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