ArticleJournal of molecular neuroscience : MN2018
TOX3 Variants Are Involved in Restless Legs Syndrome and Parkinson's Disease with Opposite Effects.
Article in Journal of molecular neuroscience : MN, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Genomic Analysis Identifies Risk Factors in Restless Legs Syndrome.Annals of neurology · 2024Pooled it
- 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
- A transcription regulator atlas identifies TOX3 as an Atoh1 coactivator in cerebellar development and tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Genomic analysis identifies risk factors in restless legs syndrome.medRxiv : the preprint server for health sciences · 2023Article
- Disrupted myelination network in the cingulate cortex of Parkinson's disease.IET systems biology · 2022Article
- Association of BST1 polymorphism with idiopathic restless legs syndrome in Chinese population.Sleep & breathing = Schlaf & Atmung · 2021Article
- Lack of Causal Effects or Genetic Correlation between Restless Legs Syndrome and Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2021Article
- Caenorhabditis elegans and its applicability to studies on restless legs syndrome.Advances in pharmacology (San Diego, Calif.) · 2019Review
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Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) and restless legs syndrome (RLS) may be clinically and/or etiologically related, yet this association is under debate. Single-nucleotide polymorphisms (SNPs) in the TOX3 gene locus were implicated in both RLS and PD genome-wide association studies (GWASs), suggesting a potential pleiotropy. Two case-control cohorts including 644 PD patients, 457 RLS patients, and 945 controls were genotyped for one known RLS-related SNP (rs3104767) and one PD-related SNP (rs4784226) in the TOX3 locus. The associations between genotype and PD and RLS risk were tested using multivariate regression models. The allele frequencies of RLS-related SNP rs3104767 in RLS patients and controls were 0.35 and 0.43, respectively (OR 0.70, p = 0.0007). Regression model suggested that this association is derived by homozygous carriage of rs3104767 (adjusted p = 0.008). A nominal association was observed for homozygous carriers of the rs3104767 SNP in PD (OR 1.62, 95% CI 1.05-2.54, p = 0.034), i.e., with an opposite direction of effect on RLS and PD, but this was not significant after Bonferroni correction. However, data from published GWASs of RLS and PD, and from the PDgene database, further supported these inverse associations. Our results confirm the association between the TOX3 SNP rs3104767 and RLS and suggest that TOX3 variants are involved in both RLS and PD, but with different or even opposite effects. Studies in larger populations of different ethnicities are required to further refine the TOX3 locus is involved in RLS and PD.
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