ReviewJournal of Parkinson's disease2024
Parkinson's Disease is Predominantly a Genetic Disease.
Review in Journal of Parkinson's disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Classification and Genotype-Phenotype Relationships of GBA1 Variants: MDSGene Systematic Review.Movement disorders : official journal of the Movement Disorder Society · 2025Pooled it
- Parkinson's disease genetics across diverse ancestries: an observational genetic study of causal and risk variants with translational implications.The Lancet. Neurology · 2026Observational
- Ex Vivo LRRK2 Activation in Asian G2385R and R1628P Variant Carriers and Idiopathic Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- Genetic and environmental risk factors of Parkinsonism.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Exploring MAPT-containing H1 and H2 haplotypes in Parkinson's disease across diverse populations.NPJ Parkinson's disease · 2026Article
- Parkinson Disease Pathogenic Variants: Cross-Ancestry Analysis and Microarray Data Validation.Neurology. Genetics · 2026Article
- One world, one goal: Advocacy and policy for a unified Parkinson's response.Journal of Parkinson's disease · 2026Review
- Review
- Genome-wide association study of copy number variations in Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Pathological Protein Targets in Parkinson's Disease: Progress Towards the Development of Disease-Modifying Therapies.CNS drugs · 2026Review
- Inflammatory signaling differentially changes chromatin accessibility and gene expression of the PD- associated kinase LRRK2 between human and mice.Molecular neurodegeneration · 2026Article
- Massive-scale single-nucleus multi-omics identifies novel rare noncoding drivers of Parkinson's disease.bioRxiv : the preprint server for biology · 2026Article
- Potential common pathogenesis of several neurodegenerative diseases.Neural regeneration research · 2026Article
- Inflammatory signaling differentially changes chromatin accessibility and gene expression of the PD- associated kinase LRRK2 between human and mice.bioRxiv : the preprint server for biology · 2026Article
- Metabolomic breath landscape analysis unravels lipid biomarker candidates in patients with genetic and idiopathic Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Neurodegeneration in Parkinson's Disease: The Role of Environmental Toxins.Journal of central nervous system disease · 2026Review
- LRRK2 p.G2385R and p.R1628P variants in a multi-ethnic Asian Parkinson's Cohort: epidemiology and clinical insights.NPJ Parkinson's disease · 2025Article
- Insulin-degrading enzyme confers neuroprotection in Parkinson's disease by inhibiting the Hippo signaling pathway.Cell death & disease · 2025Article
- Exploring MAPT-containing H1 and H2 haplotypes in Parkinson's disease across diverse populations.medRxiv : the preprint server for health sciences · 2025Article
- A multi-dimensional view on the etiology of Parkinson's disease.NPJ Parkinson's disease · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The discovery of a pathogenic variant in the alpha-synuclein (SNCA) gene in the Contursi kindred in 1997 indisputably confirmed a genetic cause in a subset of Parkinson's disease (PD) patients. Currently, pathogenic variants in one of the seven established PD genes or the strongest known risk factor gene, GBA1, are identified in ∼15% of PD patients unselected for age at onset and family history. In this Debate article, we highlight multiple avenues of research that suggest an important - and in some cases even predominant - role for genetics in PD aetiology, including familial clustering, high rates of monogenic PD in selected populations, and complete penetrance with certain forms. At first sight, the steep increase in PD prevalence exceeding that of other neurodegenerative diseases may argue against a predominant genetic etiology. Notably, the principal genetic contribution in PD is conferred by pathogenic variants in LRRK2 and GBA1 and, in both cases, characterized by an overall late age of onset and age-related penetrance. In addition, polygenic risk plays a considerable role in PD. However, it is likely that, in the majority of PD patients, a complex interplay of aging, genetic, environmental, and epigenetic factors leads to disease development.
Indexed as
Identifiers
What OpenQuestion holds
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.