ArticleAging2024
Joint analysis of proteome, transcriptome, and multi-trait analysis to identify novel Parkinson's disease risk genes.
Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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.
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- Integrative TWAS and multi-omics analyses prioritize HSPE1 as a candidate risk gene for bipolar disorder with immune cell-specific regulatory evidence.European archives of psychiatry and clinical neuroscience · 2026Article
- Cell-type-specific genetic architecture reveals neuronal and immune contributions to neuropsychiatric disorders.Molecular psychiatry · 2026Article
- Integrating dorsolateral prefrontal cortex multi-omics and GWAS summary data reveals genetic etiology of Parkinson's disease.Research square · 2026Article
- Integrating dorsolateral prefrontal cortex multi-omics and GWAS summary data reveals genetic etiology of Parkinson's disease.medRxiv : the preprint server for health sciences · 2026Article
- NADAlzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Integrative transcriptome-wide association analyses reveal PRKCG-linked GABAergic dysfunction in Fragile X-associated tremor/ataxia syndrome.Nature communications · 2026Article
- Immune Cell Proteins and Parkinson's Disease: A Mendelian Randomization Analysis of Causal Associations.Brain and behavior · 2025Article
- Multitrait Genetic Analysis Identifies Novel Pleiotropic Loci for Depression and Schizophrenia in East Asians.Schizophrenia bulletin · 2025Article
- Gaining new insights into the etiology of ulcerative colitis through a cross-tissue transcriptome-wide association study.Frontiers in genetics · 2024Article
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genome-wide association studies (GWAS) have identified multiple risk variants for Parkinson's disease (PD). Nevertheless, how the risk variants confer the risk of PD remains largely unknown. We conducted a proteome-wide association study (PWAS) and summary-data-based mendelian randomization (SMR) analysis by integrating PD GWAS with proteome and protein quantitative trait loci (pQTL) data from human brain, plasma and CSF. We also performed a large transcriptome-wide association study (TWAS) and Fine-mapping of causal gene sets (FOCUS), leveraging joint-tissue imputation (JTI) prediction models of 22 tissues to identify and prioritize putatively causal genes. We further conducted PWAS, SMR, TWAS, and FOCUS using a multi-trait analysis of GWAS (MTAG) to identify additional PD risk genes to boost statistical power. In this large-scale study, we identified 16 genes whose genetically regulated protein abundance levels were associated with Parkinson's disease risk. We undertook a large-scale analysis of PD and correlated traits, through TWAS and FOCUS studies, and discovered 26 casual genes related to PD that had not been reported in previous TWAS. 5 genes (
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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.