ArticleBrain sciences2023
Genetics of Neurogenic Orthostatic Hypotension in Parkinson's Disease, Results from a Cross-Sectional In Silico Study.
Article in Brain sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Prevalence and impact of orthostatic hypotension in Parkinson's disease: a systematic review and meta-analysis.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2025Pooled it
- Eating Disorders and Parkinson's Disease-2: Genetic Epidemiology and Shared Genomics.European eating disorders review : the journal of the Eating Disorders Association · 2026Article
- How to treat cardiovascular autonomic failure in Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Eating Disorders and Parkinson's Disease - 2: Population Burden, Genetic Epidemiology and Shared Genomics.medRxiv : the preprint server for health sciences · 2026Article
- Dual-Omics Mapping of Tinnitus Phenotype Transition in Noise-Exposed Auditory Cortex.Cellular and molecular neurobiology · 2025Article
- Review
- MicroRNAs and rs1803274 SNP-based BuChe downregulation are associated with metabolic syndrome through ghrelin hydrolysis and expression quantitative trait loci regulation in PD patients.Frontiers in molecular neuroscience · 2025Article
- Longitudinal prevalence of neurogenic orthostatic hypotension in the idiopathic Parkinson Progression Marker Initiative (PPMI) cohort.Autonomic neuroscience : basic & clinical · 2024Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The genetic basis of Neurogenic Orthostatic Hypotension (NOH) in Parkinson's disease (PD) has been inadequately explored. In a cross-sectional study, we examined the association between NOH and PD-related single-nucleotide polymorphisms (SNPs) and mapped their effects on gene expression and metabolic and signaling pathways. Patients with PD, free from pathological conditions associated with OH, and not taking OH-associated medications were included. NOH was defined as per international guidelines. Logistic regression was used to relate SNPs to NOH. Linkage-disequilibrium analysis, expression quantitative trait loci, and enrichment analysis were used to assess the effects on gene expression and metabolic/signaling pathways. We included 304 PD patients in the study, 35 of whom had NOH (11.5%). NOH was more frequent in patients with SNPs in SNCA, TMEM175, FAM47E-STBD1, CCDC62, SCN3A, MIR4696, SH3GL2, and LZTS3/DDRGK1 and less frequent in those with SNPs in ITGA8, IP6K2, SIPA1L2, NDUFAF2. These SNPs affected gene expression associated with the significant hierarchical central structures of the autonomic nervous system. They influenced several metabolic/signaling pathways, most notably IP3/Ca++ signaling, the PKA-CREB pathway, and the metabolism of fatty acids. These findings provide new insights into the pathophysiology of NOH in PD and may provide targets for future therapies.
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