ArticleNPJ Parkinson's disease2023
Expanding causal genes for Parkinson's disease via multi-omics analysis.
Article in NPJ Parkinson's disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Multi-omics and high-spatial-resolution omics: deciphering complexity in neurological disorders.GigaScience · 2025Pooled it
- Artificial intelligence and multiomics integration for Parkinson's disease drug development.Molecules and cells · 2026Review
- Human CSF proteogenomics links genetic variation to neurodegenerative disease proteins.medRxiv : the preprint server for health sciences · 2026Article
- Biological aging predicts mortality in Parkinson's patients: evidence from UK Biobank.NPJ Parkinson's disease · 2026Article
- Neuroinflammation and metabolic reprogramming in Parkinson's disease.Frontiers in immunology · 2026Review
- Integrated Multi-Omics Profiling Identifies CD84-Associated Microglial Alterations in Focal Cortical Dysplasia Type II.Journal of inflammation research · 2026Article
- Causal Implication of CD52-Driven Immune Dysregulation in Sarcopenic Obesity: Integrating Mendelian Randomization and Multiomics Profiling.Clinical interventions in aging · 2026Article
- CD38-NAD(+) Axis: New Insights into Glaucoma Therapy.Molecular neurobiology · 2025Review
- Synergistic blood-based diagnostic value of AP3B1 and BMPR2 in Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Identifying Key Plasma Proteins in the Onset of Parkinson's Disease: Proteome-Wide Mendelian Randomization and Single-Cell RNA Sequencing Analysis.Molecular neurobiology · 2025Article
- Systematic Exploration of Potential Druggable Genes for Ischemic Stroke Employing Genome-Wide Mendelian Randomization Analysis.Brain and behavior · 2025Article
- Integration of multi-omics quantitative trait loci evidence reveals novel susceptibility genes for Alzheimer's disease.Scientific reports · 2025Article
- Aberrant humoral immune responses and intestinal homeostasis in Cd38 Bst1 double knockout mice.ImmunoHorizons · 2025Article
- A community-led initiative to de-risk and advance Parkinson's disease therapeutic targets.NPJ Parkinson's disease · 2025Review
- Multi-omics machine learning classifier and blood transcriptomic signature of Parkinson's disease.Research square · 2025Article
- Investigating potential drug targets for the treatment of glioblastoma: a Mendelian randomization study.BMC cancer · 2025Article
- Characterization of Isolated Human Astrocytes from Aging Brain.International journal of molecular sciences · 2025Article
- Article
- Association of 25-hydroxyvitamin D with Parkinson's disease based on the results from the NHANES 2007 to 2018 and Mendelian randomization analysis.Scientific reports · 2025Article
- Proteome-Wide Association Study for Finding Druggable Targets in Progression and Onset of Parkinson's Disease.CNS neuroscience & therapeutics · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genome‑wide association studies (GWASs) have revealed numerous loci associated with Parkinson's disease (PD). However, some potential causal/risk genes were still not revealed and no etiological therapies are available. To find potential causal genes and explore genetically supported drug targets for PD is urgent. By integrating the expression quantitative trait loci (eQTL) and protein quantitative trait loci (pQTL) datasets from multiple tissues (blood, cerebrospinal fluid (CSF) and brain) and PD GWAS summary statistics, a pipeline combing Mendelian randomization (MR), Steiger filtering analysis, Bayesian colocalization, fine mapping, Protein-protein network and enrichment analysis were applied to identify potential causal genes for PD. As a result, GPNMB displayed a robust causal role for PD at the protein level in the blood, CSF and brain, and transcriptional level in the brain, while the protective role of CD38 (in brain pQTL and eQTL) was also identified. We also found inconsistent roles of DGKQ on PD between protein and mRNA levels. Another 9 proteins (CTSB, ARSA, SEC23IP, CD84, ENTPD1, FCGR2B, BAG3, SNCA, FCGR2A) were associated with the risk for PD based on only a single pQTL after multiple corrections. We also identified some proteins' interactions with known PD causative genes and therapeutic targets. In conclusion, this study suggested GPNMB, CD38, and DGKQ may act in the pathogenesis of PD, but whether the other proteins involved in PD needs more evidence. These findings would help to uncover the genes underlying PD and prioritize targets for future therapeutic interventions.
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.