{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,30]],"date-time":"2025-07-30T16:27:18Z","timestamp":1753892838874,"version":"3.41.2"},"reference-count":59,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2024,7,9]],"date-time":"2024-07-09T00:00:00Z","timestamp":1720483200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Psychiatry"],"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Research from observational studies has demonstrated a link between Alzheimer\u2019s disease (AD) and a higher risk of cardiovascular disease (CVD). Uncertainty surrounds the exact genetic cause of AD and coronary heart disease, particularly unstable angina (UA). Mendelian randomization (MR) analysis was used to examine the causal genetic link between AD and UA to evaluate the impact of AD on UA.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The purpose of the bidirectional MR analysis was to investigate the link between exposure and illness causation. Genetic instrumental variables for AD were obtained from European populations using genome-wide association studies (GWAS). The primary causal conclusions were obtained using the inverse variance weighted approach (IVW), and other sensitivity analysis techniques were employed. Sensitivity analyses were carried out to evaluate heterogeneity and horizontal pleiotropy to guarantee accurate MR results.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>An elevated risk of UA was linked to genetically predicted AD (IVW: OR=3.439, 95% CI: 1.565-7.555, P=0.002). A substantial genetic relationship between UA and the risk of AD was not supported by any evidence in the reverse study (IVW: OR=0.998, 95% CI: 0.995-1.001, P=0.190). Various MR techniques produced consistent results. Sensitivity analysis revealed no discernible heterogeneity or horizontal pleiotropy.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>One risk factor for UA that we found in our bidirectional Mendelian randomization trial was AD. This highlights the necessity of researching the underlying molecular mechanisms linked to AD and UA as well as the possibility of creating individualized treatment plans based on genetic data.<\/jats:p><\/jats:sec>","DOI":"10.3389\/fpsyt.2024.1435394","type":"journal-article","created":{"date-parts":[[2024,7,9]],"date-time":"2024-07-09T04:49:06Z","timestamp":1720500546000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Causal relationship between Alzheimer\u2019s disease and unstable angina: a bidirectional Mendelian randomization 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