ArticlePloS one2017
Parkinson's disease-associated genetic variation is linked to quantitative expression of inflammatory genes.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 42 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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
42 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Using iPSC models to examine neuron-glia interactions in neurodegenerative diseases.Bioscience reports · 2026Review
- Shared Epitope-PositiveNeurology(R) neuroimmunology & neuroinflammation · 2026Article
- Microglia heterogeneity and therapeutic strategies in Parkinson's disease.Frontiers in immunology · 2026Review
- Age-related nigral downregulation of the Parkinson's risk factor FAM49B primes human microglia for inflammaging.npj aging · 2025Article
- Association of Peripheral Blood Neutrophil-Lymphocyte Ratio With Motor and Cognitive Function in Prodromal Parkinson's Disease.Brain and behavior · 2025Article
- OPTN protects retinal ganglion cells and ameliorates neuroinflammation in optic neuropathies.Communications biology · 2025Article
- Article
- Peripheral endotoxin exposure in mice activates crosstalk between phagocytes in the brain and periphery.Research square · 2024Article
- An overview on microglial origin, distribution, and phenotype in Alzheimer's disease.Journal of cellular physiology · 2024Review
- Nigrostriatal degeneration determines dynamics of glial inflammatory and phagocytic activity.Journal of neuroinflammation · 2024Article
- Modeling the neuroimmune system in Alzheimer's and Parkinson's diseases.Journal of neuroinflammation · 2024Review
- Emergence of the brain-border immune niches and their contribution to the development of neurodegenerative diseases.Frontiers in immunology · 2024Review
- Microfluidics-free single-cell genomics reveals complex central-peripheral immune crosstalk in the mouse brain during peripheral inflammation.Research square · 2023Article
- Pathological mechanisms of neuroimmune response and multitarget disease-modifying therapies of mesenchymal stem cells in Parkinson's disease.Stem cell research & therapy · 2023Review
- Microglia and Astrocytes Dysfunction and Key Neuroinflammation-Based Biomarkers in Parkinson's Disease.Brain sciences · 2023Review
- The Interplay between α-Synuclein and Microglia in α-Synucleinopathies.International journal of molecular sciences · 2023Review
- Pathogenesis of α-Synuclein in Parkinson's Disease: From a Neuron-Glia Crosstalk Perspective.International journal of molecular sciences · 2022Review
- Environmental pathways affecting gene expression (E.PAGE) as an R package to predict gene-environment associations.Scientific reports · 2022Article
- Inflammation and immune dysfunction in Parkinson disease.Nature reviews. Immunology · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genome-wide association studies (GWAS) have linked dozens of single nucleotide polymorphisms (SNPs) with Parkinson's disease (PD) risk. Ascertaining the functional and eventual causal mechanisms underlying these relationships has proven difficult. The majority of risk SNPs, and nearby SNPs in linkage disequilibrium (LD), are found in intergenic or intronic regions and confer risk through allele-dependent expression of multiple unknown target genes. Combining GWAS results with publicly available GTEx data, generated through eQTL (expression quantitative trait loci) identification studies, enables a direct association of SNPs to gene expression levels and aids in narrowing the large population of potential genetic targets for hypothesis-driven experimental cell biology. Separately, overlapping of SNPs with putative enhancer segmentations can strengthen target filtering. We report here the results of analyzing 7,607 PD risk SNPs along with an additional 23,759 high linkage disequilibrium-associated variants paired with eQTL gene expression. We found that enrichment analysis on the set of genes following target filtering pointed to a single large LD block at 6p21 that contained multiple HLA-MHC-II genes. These MHC-II genes remain associated with PD when the genes were filtered for correlation between GWAS significance and eQTL levels, strongly indicating a direct effect on PD etiology.
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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.