Causality relationship between 91 inflammatory factors and Alzheimer disease: A bidirectional Mendelian randomization
Qijia Li1, Shunyou Jing1, Ning Li1
1Department of Clinical Laboratory, Sichuan Provincial Women's and Children's Hospital/The Affiliated Women's and Children's Hospital of Chengdu Medical College, Chengdu, China.
Medicine
|May 4, 2026
Summary
This study used Mendelian randomization to explore links between systemic inflammation and Alzheimer disease (AD). Certain inflammatory factors may increase AD risk, while others appear to be consequences of the disease.
Area of Science:
- Neuroscience
- Immunology
- Genetics
Background:
- Alzheimer disease (AD) is a complex neurodegenerative disorder linked to systemic inflammation.
- Understanding the interplay between inflammation and AD is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the causal relationship between systemic inflammatory factors and Alzheimer disease.
- To identify potential biomarkers and therapeutic targets for AD.
Main Methods:
- Utilized a bidirectional Mendelian randomization (MR) design.
- Incorporated aggregated data from large-scale genome-wide association studies (GWAS).
Main Results:
- Identified nine systemic inflammatory factors causally associated with increased AD risk, including interleukin-6 and tumor necrosis factor.
- Found five circulating inflammatory factors, such as cystatin D and monocyte chemoattractant protein-4, to be downstream consequences of AD.
- Highlighted novel roles for cystatin D and monocyte chemoattractant protein-4 in AD pathogenesis.
Conclusions:
- Systemic inflammation plays a significant role in Alzheimer disease development and progression.
- Specific inflammatory factors may serve as novel biomarkers or therapeutic targets for AD.
- Further research into these inflammatory pathways could advance AD diagnosis and treatment.
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