Background: This study aims to explore the causal relationship between five selected factors-, , , , and -and early-onset Alzheimer's disease (EOAD) through related genes, providing clues for EOAD research.
Methods: Using genes related to the five selected factors as exposure variables and EOAD as the disease outcome, significant genes were screened through Mendelian randomization (MR) analysis using the inverse-variance weighted (IVW) method, based on the OpenGWAS database. The selected genes were intersected with genes related to the exposure factors to assess the causal relationships between the five factors and EOAD.
Results: MR analysis identified 13 genes in total. Six of these genes were protective factors for EOAD, with LYST being the most significant (OR = 0.4259, 95% CI: 0.2218-0.8178, p = 0.0103). Seven genes were risk factors for EOAD, with NCF4 being the most significant (OR = 2.7207, 95% CI: 1.0229-7.2362, p = 0.0449). A total of 1925 genes related to , , , , and were analyzed. After intersection, 10 lysosome-related genes (NCF4, VIPAS39, LYST, SORT1, ARSB, EPDR1, SYNGR1, ANXA11, PYGB, CLN5) and 3 endothelium cell -related genes (ADM, NFIB, NKTR) were found to have significant causal relationships with EOAD.
Conclusions: There are genes related to and that have significant relationships with EOAD, while no causal relationships were found between , , , and EOAD. This study provides an important basis for further EOAD research.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1177/13872877241310248 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
It is known that inhibition of the endoplasmic reticulum transmembrane signaling protein (ERN1) suppresses the glioblastoma cells proliferation. The present study aims to investigate the impact of inhibition of ERN1 endoribonuclease and protein kinase activities on the , , and gene expression in U87MG glioblastoma cells with an intent to reveal the role of ERN1 signaling in the regulation of expression of these genes. The U87MG glioblastoma cells with inhibited ERN1 endoribonuclease (dnrERN1) or both enzymatic activities of ERN1 (endoribonuclease and protein kinase; dnERN1) were used.
View Article and Find Full Text PDFGenetic factors contribute to the development of metabolic syndrome and subsequent arterial hypertension (AH). The study of the T786C polymorphism of the endothelial nitric oxide synthase (eNOS) gene in arterial hypertension is important as its correlation with adipokine imbalance is a novelty area to find associations between hypertension development, obesity, and heredity. The purpose of the current study was to investigate serum adipokines levels, depending on the T786C polymorphism of the eNOS in patients with arterial hypertension.
View Article and Find Full Text PDFImpact of obesity on the CCR6-CCL20 axis in epidermal γδ T cells and IL-17A production in murine wound healing and psoriasis.
J Immunol
January 2025
Department of Biological Sciences, California State University San Marcos, San Marcos, CA, United States.
Obesity is associated with comorbidities including type 2 diabetes, chronic nonhealing wounds, and psoriasis. Normally, skin homeostasis and repair is regulated through the production of cytokines and growth factors derived from skin-resident cells including epidermal γδ T cells. However, epidermal γδ T cells exhibit reduced proliferation and defective growth factor and cytokine production during obesity and type 2 diabetes.
View Article and Find Full Text PDFPlasmacytoid dendritic cell sensing of African swine fever virus-infected macrophages results in STING-dependent robust interferon-α production.
J Immunol
January 2025
Institute of Virology and Immunology, Mittelhäusern, Switzerland.
While several African swine fever virus (ASFV)-encoded proteins potently interfere with the cGAS-STING (cyclic GMP-AMP synthetase-stimulator of interferon genes) pathway at different levels to suppress interferon (IFN) type I production in infected macrophages, systemic IFN-α is induced during the early stages of AFSV infection in pigs. The present study elucidates a mechanism by which such responses can be triggered, at least in vitro. We demonstrate that infection of monocyte-derived macrophages (MDMs) by ASFV genotype 2 strains is highly efficient but immunologically silent with respect to IFN type I, IFN-stimulated gene induction, and tumor necrosis factor production.
View Article and Find Full Text PDFRapid clonal expansion and somatic hypermutation contribute to the fate of SARS-CoV-2 broadly neutralizing antibodies.
J Immunol
February 2025
Institute for Hepatology, National Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, The Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen, Guangdong Province, China.
Several vaccines and immunization strategies, including inactivated vaccines, have proven effective in eliciting antibodies against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), providing an opportunity to characterize the antibody response. In this study, we investigated the monoclonal antibody responses elicited by wild-type SARS-CoV-2 inactivated vaccination compared to those elicited by natural infection and mRNA vaccination. The analysis showed that antibodies encoded by biased germline genes were shared between SARS-CoV-2 vaccinated and naturally infected individuals.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!