Jared M Phillips, Julie A Schneider, David A Bennett, Paul K Crane, Shannon L Risacher, Andrew J Saykin, Logan C Dumitrescu, Timothy J Hohman
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We hypothesized that an astrocyte activation PRS could aid in the early detection of faster clinical decline. Therefore, we constructed an astrocyte activation PRS and assessed its predictive value for cognitive decline and AD biomarkers (i.e., cerebrospinal fluid [CSF] levels of Aβ1-42, total tau, and p-tau181) in a cohort of 791 elderly individuals. The astrocyte activation PRS showed significant main effects on cross-sectional memory (β = -0.07, p = 0.03) and longitudinal executive function (β = -0.01, p = 0.03). Additionally, the PRS interacted with amyloid positivity (p.intx = 0.02), whereby indicating that amyloid burden modifies the association between the PRS and annual rate of language decline. Furthermore, the PRS was negatively associated with CSF Aβ1-42 levels (β = -3.4, p = 0.07) and interacted with amyloid status, such that amyloid burden modifies the association between the PRS and CSF phosphorylated tau levels (p.intx = 0.08). These findings suggest that an astrocyte activation PRS could be a valuable tool for early disease risk prediction, potentially enabling intervention during the interval between pathogenic amyloid and tau accumulation.</p>","PeriodicalId":34954,"journal":{"name":"Pacific Symposium on Biocomputing. 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引用次数: 0
摘要
阿尔茨海默病(AD)是一种多基因疾病,前驱期延长,使早期诊断复杂化。最近的研究表明,星形胶质细胞反应性增加与致病性tau积聚的高风险相关,特别是在淀粉样蛋白阳性个体中。然而,很少有临床工具可用于预测哪些个体可能表现出升高的星形胶质细胞激活,从而易受过度磷酸化tau诱导的神经变性的影响。多基因风险评分(PRS)综合了多个基因位点的影响,提供了一个单一的、连续的指标,代表了个体对特定表型的遗传风险。我们假设星形胶质细胞激活PRS可以帮助早期发现更快的临床衰退。因此,我们在791名老年人中构建了星形胶质细胞激活PRS,并评估了其对认知能力下降和AD生物标志物(即脑脊液中a β1-42、总tau和p-tau181)的预测价值。星形胶质细胞激活对横截面记忆(β = -0.07, p = 0.03)和纵向执行功能(β = -0.01, p = 0.03)有显著的主要影响。此外,PRS与淀粉样蛋白阳性相互作用(p.intx = 0.02),这表明淀粉样蛋白负担改变了PRS与年语言衰退率之间的关系。此外,PRS与脑脊液Aβ1-42水平呈负相关(β = -3.4, p = 0.07),并与淀粉样蛋白状态相互作用,因此淀粉样蛋白负荷改变了PRS与脑脊液磷酸化tau水平之间的关系(p.intx = 0.08)。这些发现表明星形胶质细胞激活PRS可能是早期疾病风险预测的一个有价值的工具,可能在致病性淀粉样蛋白和tau积累之间的间隔期间进行干预。
Astrocyte Reactivity Polygenic Risk Score May Predict Cognitive Decline in Alzheimer's Disease.
Alzheimer's disease (AD) is a polygenic disorder with a prolonged prodromal phase, complicating early diagnosis. Recent research indicates that increased astrocyte reactivity is associated with a higher risk of pathogenic tau accumulation, particularly in amyloid-positive individuals. However, few clinical tools are available to predict which individuals are likely to exhibit elevated astrocyte activation and, consequently, be susceptible to hyperphosphorylated tau-induced neurodegeneration. Polygenic risk scores (PRS) aggregate the effects of multiple genetic loci to provide a single, continuous metric representing an individual's genetic risk for a specific phenotype. We hypothesized that an astrocyte activation PRS could aid in the early detection of faster clinical decline. Therefore, we constructed an astrocyte activation PRS and assessed its predictive value for cognitive decline and AD biomarkers (i.e., cerebrospinal fluid [CSF] levels of Aβ1-42, total tau, and p-tau181) in a cohort of 791 elderly individuals. The astrocyte activation PRS showed significant main effects on cross-sectional memory (β = -0.07, p = 0.03) and longitudinal executive function (β = -0.01, p = 0.03). Additionally, the PRS interacted with amyloid positivity (p.intx = 0.02), whereby indicating that amyloid burden modifies the association between the PRS and annual rate of language decline. Furthermore, the PRS was negatively associated with CSF Aβ1-42 levels (β = -3.4, p = 0.07) and interacted with amyloid status, such that amyloid burden modifies the association between the PRS and CSF phosphorylated tau levels (p.intx = 0.08). These findings suggest that an astrocyte activation PRS could be a valuable tool for early disease risk prediction, potentially enabling intervention during the interval between pathogenic amyloid and tau accumulation.