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

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 causa...

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Autores principales: Tsui, Alex, Davis, Daniel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6640034/
https://www.ncbi.nlm.nih.gov/pubmed/31328178
http://dx.doi.org/10.1002/agm2.12046
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author Tsui, Alex
Davis, Daniel
author_facet Tsui, Alex
Davis, Daniel
author_sort Tsui, Alex
collection PubMed
description 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.
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spelling pubmed-66400342019-07-19 Systemic inflammation and causal risk for Alzheimer's dementia: Possibilities and limitations of a Mendelian randomization approach Tsui, Alex Davis, Daniel Aging Med (Milton) Original Articles 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. John Wiley and Sons Inc. 2018-12-05 /pmc/articles/PMC6640034/ /pubmed/31328178 http://dx.doi.org/10.1002/agm2.12046 Text en © 2018 The Authors. Aging Medicine published by Beijing Hospital and John Wiley & Sons Australia, Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Tsui, Alex
Davis, Daniel
Systemic inflammation and causal risk for Alzheimer's dementia: Possibilities and limitations of a Mendelian randomization approach
title Systemic inflammation and causal risk for Alzheimer's dementia: Possibilities and limitations of a Mendelian randomization approach
title_full Systemic inflammation and causal risk for Alzheimer's dementia: Possibilities and limitations of a Mendelian randomization approach
title_fullStr Systemic inflammation and causal risk for Alzheimer's dementia: Possibilities and limitations of a Mendelian randomization approach
title_full_unstemmed Systemic inflammation and causal risk for Alzheimer's dementia: Possibilities and limitations of a Mendelian randomization approach
title_short Systemic inflammation and causal risk for Alzheimer's dementia: Possibilities and limitations of a Mendelian randomization approach
title_sort systemic inflammation and causal risk for alzheimer's dementia: possibilities and limitations of a mendelian randomization approach
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6640034/
https://www.ncbi.nlm.nih.gov/pubmed/31328178
http://dx.doi.org/10.1002/agm2.12046
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