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Systemic inflammation and causal risk for Alzheimer’s dementia: Possibilities and limitations of a Mendelian randomization approach

机译:全身性炎症和阿尔茨海默氏症的病因风险:孟德尔随机方法的可能性和局限性

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摘要

Epidemiological studies have implicated systemic inflammation in the development of Alzheimer’s disease (AD). However, these observations have been subject to residual confounding and reverse causation. We applied Mendelian randomization approaches to address this. We did not identify any causal associations between serum interleukin (IL)-18, IL-1ra, IL-6, or erythrocyte sedimentation rate (ESR) concentrations and AD. Our findings are limited by the low number of available instruments, though some of those identified (e.g., IL-6) were of sufficient power to indicate true negative results. Taken together, it appears there is no evidence for a causal association between these serum inflammatory cytokines and AD.
机译:流行病学研究表明全身性炎症与阿尔茨海默氏病(AD)的发展有关。但是,这些观察结果容易产生混淆和反因果关系。我们应用孟德尔随机化方法来解决这个问题。我们没有发现血清白介素(IL)-18,IL-1ra,IL-6或红细胞沉降率(ESR)浓度与AD之间有任何因果关系。尽管发现的某些仪器(例如IL-6)具有足够的能力指示真正的阴性结果,但我们的研究结果受到可用仪器数量的限制。两者合计,似乎没有证据表明这些血清炎性细胞因子与AD之间存在因果关系。

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