Background: The global outbreak of COVID-19, caused by the SARS-CoV-2 virus, has been linked to long-term neurological complications, including Alzheimer's disease (AD) among seniors. However, the precise genetic impact of COVID-19 on long-term AD development remains unclear.
Method: This study leveraged genome-wide association study (GWAS) data and genotype data to explore the genetic correlation between AD and various COVID-19 phenotypes across European ancestry (EA) and African ancestry (AA). We first calculated the polygenic risk scores (PRSs) of three COVID-19 phenotypes in AD cases and controls from both EA and AA populations, then determined the genetic correlations between COVID-19 PRSs and AD by logistic regression analyses with or without adjusting for age, sex, and APOE genotypes. Furthermore, shared SNPs and genes were identified through variant mapping and gene annotation from the large GWAS data of both diseases.
Result: Our study identified significant positive correlations between AD diagnosis and COVID-19 in both populations. Notably, correlations were stronger from AA as compared to the EA population. In addition, significant shared variants and genes were identified in the chr17q21.31 region, suggesting common biological mechanisms may contribute to the high comorbidity between AD and COVID-19.
Conclusion: Further functional studies are required to understand their causal relationships, leading to enhanced prevention and treatments for both conditions.
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http://dx.doi.org/10.1002/alz.086755 | DOI Listing |
HGG Adv
January 2025
Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Inherited genetics represents an important contributor to risk of esophageal adenocarcinoma (EAC), and its precursor Barrett's esophagus (BE). Genome-wide association studies have identified ∼30 susceptibility variants for BE/EAC, yet genetic interactions remain unexamined. To address challenges in large-scale G×G scans, we combined knowledge-guided filtering and machine learning approaches, focusing on genes with (A) known/plausible links to BE/EAC pathogenesis (n=493) or (B) prior evidence of biological interactions (n=4,196).
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Observational studies have shown that the risk of developing herpes zoster (HZ) increases with the use of statins. However, there are many confounding factors in observational studies. Therefore, our Mendelian randomization (MR) study aimed to explore the causal role of lipids in HZ and to assess the causal impact of lipid-lowering drug targets on HZ risk.
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January 2025
Department of Neurology, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, Guangxi, China.
Benign paroxysmal vertigo (BPV) is a common cause of dizziness, and some patients are comorbid with psychiatric disorders such as depression, requiring intervention with antidepressants. However, the causal association between BPV, depression and antidepressants has not been clearly established. We used two-sample bidirectional Mendelian randomization (MR) to analyze the causal association between BPV, depression, and antidepressants.
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January 2025
Department of Epidemiology and Biostatistics, School of Public Health, Southeast University, Nanjing, People's Republic of China.
Previous observational studies have reported inconsistent associations between nut consumption and cardiovascular diseases (CVD). This study aims to identify the causal relationship between different types of nuts consumption and CVD, and to quantify the potential mediating effects of cardiometabolic factors. We utilized Genome-Wide Association Study (GWAS) data to assess the causal effects of nut consumption on CVD using two-sample Mendelian randomization (MR) and a two-step MR analysis.
View Article and Find Full Text PDFTransl Psychiatry
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Genetic Epidemiology Group, Department of Psychiatry, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Experiencing a traumatic event may lead to Posttraumatic Stress Disorder (PTSD), including symptoms such as flashbacks and hyperarousal. Individuals suffering from PTSD are at increased risk of cardiovascular disease (CVD), but it is unclear why. This study assesses shared genetic liability and potential causal pathways between PTSD and CVD.
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