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Research Paper|Volume 15, Issue 17|pp 9022—9040

Causal relationship between Alzheimer’s disease and cardiovascular disease: a bidirectional Mendelian randomization analysis

Fengjun Zhang1, Dexian Xian1, Junchen Feng2, Luning Ning1, Tianshou Jiang3, Wenchang Xu1, Yuan Liu4, Qiong Zhao4, Min Peng4
  • 1College of Acupuncture and Massage, Shandong University of Traditional Chinese Medicine, Jinan, China
  • 2College of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China
  • 3Department of Cardiovascular Medicine, Lacey City Hospital, Qingdao, China
  • 4Department of Traditional Chinese Medicine, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China
* Equal contribution
Received: February 4, 2023Accepted: August 22, 2023Published: September 2, 2023
https://doi.org/10.18632/aging.205013

Copyright: © 2023 Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Observational studies suggest that cardiovascular disease (CVD) increases the risk of developing Alzheimer’s disease (AD). However, the causal relationship between the two is not clear. This study applied a two-sample bidirectional Mendelian randomization method to explore the causal relationship between CVD and AD. Genome-wide association study (GWAS) data from 46 datasets of European populations (21,982 cases of AD and 41,944 controls) were utilized to obtain genetic instrumental variables for AD. In addition, genetic instrumental variables for atrial fibrillation (AF), heart failure (HF), myocardial infarction (MI), coronary heart disease (CHD), angina pectoris (AP), and ischemic stroke (IS) (including large-artery atherosclerotic stroke [LAS] and cardioembolic stroke [CES]) were selected from GWAS data of European populations (P < 5E-8). The inverse variance weighting method was employed as the major Mendelian randomization analysis method. Genetically predicted AD odds ratios (OR) (1.06) (95% CI: 1.02–1.10, P = 0.003) were linked to higher AP analysis. A higher genetically predicted OR for CES (0.9) (95% CI 0.82–0.99, P = 0.02) was linked to a decreased AD risk. This Mendelian randomized study identified AD as a risk factor for AP. In addition, CES was related to a reduced incidence of AD. Therefore, these modifiable risk factors are crucial targets for preventing and treating AD.