ArticleNPJ Parkinson's disease2024
Discovering genetic mechanisms underlying the co-occurrence of Parkinson's disease and non-motor traits.
Article in NPJ Parkinson's disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
The trial behind it
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Variant-to-function dissection of the 17q21.31 locus resolves ANKRD1 as a convergent regulatory target.BMC medical genomics · 2026Article
- Inherited Genetic Variation in Parkinson's Disease: Convergence on Impaired Autophagosome-Lysosome Fusion Through the Altered Expression of mRNA Isoforms.Molecular neurobiology · 2025Article
- Review
- Identification of 27 allele-specific regulatory variants in Parkinson's disease using a massively parallel reporter assay.NPJ Parkinson's disease · 2024Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding the biological mechanisms that underlie the non-motor symptoms of Parkinson's disease (PD) requires comprehensive frameworks that unravel the complex interplay of genetic risk factors. Here, we used a disease-agnostic brain cortex gene regulatory network integrated with Mendelian Randomization analyses that identified 19 genes whose changes in expression were causally linked to PD. We further used the network to identify genes that are regulated by PD-associated genome-wide association study (GWAS) SNPs. Extended protein interaction networks derived from PD-risk genes and PD-associated SNPs identified convergent impacts on biological pathways and phenotypes, connecting PD with established co-occurring traits, including non-motor symptoms. These findings hold promise for therapeutic development. In conclusion, while distinct sets of genes likely influence PD risk and outcomes, the existence of genes in common and intersecting pathways associated with other traits suggests that they may contribute to both increased PD risk and symptom heterogeneity observed in people with Parkinson's.
Identifiers
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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 OpenQuestion graph.