Open AccessSystemic inflammation and causal risk for Alzheimer's dementia: Possibilities and limitations of a Mendelian randomization approach
Author(s) -
Tsui Alex,
Davis Daniel
Publication year - 2018
Publication title -
aging medicine
Language(s) - English
Resource type - Journals
ISSN - 2475-0360
DOI - 10.1002/agm2.12046
Subject(s) - mendelian randomization , confounding , systemic inflammation , dementia , causation , disease , inflammation , causal inference , medicine , alzheimer's disease , causality (physics) , epidemiology , erythrocyte sedimentation rate , immunology , bioinformatics , psychology , biology , pathology , gene , genetics , physics , quantum mechanics , genetic variants , genotype , political science , law
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 .