ArticleMolecular neurobiology2025
Double-Negative CD4 CD8 Absolute Count Plays a Mediating Role in the Causal Relationship Between Plasma Lipids and Parkinson's Disease: A Mendel Randomized Study.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Immunosenescence and inflammaging in Parkinson's disease: mechanisms and therapeutic prospects.Frontiers in immunology · 2026Review
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
According to certain research, there might be a connection between Parkinson's disease and plasma lipidome. However, the causal effects between plasma lipidome and Parkinson's disease and whether immune cells act as a mediator remain unclear. According to some research, plasma lipids are an important risk factor for Parkinson's disease, however, whether there is a causative connection between the two is unclear. In this study, Mendelian randomization (MR) was utilized to investigate the causal effect of plasma lipidomics on Parkinson's disease while conducting mediation analysis to determine whether immune cells served as mediators in this association. Plasma lipidome, immune cells, and Parkinson's disease were identified from large-scale genome-wide association studies (GWAS) summary data. We explored the causal connections between the plasma lipidome, Parkinson's disease, and the immune system using Mendelian randomization (MR). Inverse variance weighting (IVW) was used as the main statistical method. Furthermore, we investigated the potential that immune cells play a mediating role in the pathway leading from the plasma lipidome to Parkinson's disease. There were two positive and four negative causal effects between genetic liability in the plasma lipidome and Parkinson's disease. In addition, there were four positive and three negative causal relationships between immune cells and Parkinson's disease. The immune cells function as a mediator. Immune cells functioned as mediating components in the pathway from plasma lipidome to Parkinson's disease, and both plasma lipidome and immune cells were causally related to Parkinson's disease. It is expected that immune cells and plasma lipid intervention can be used as a preventive and therapeutic strategy for Parkinson's disease.
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