ReviewNeuroscience2019
Contributions of VPS35 Mutations to Parkinson's Disease.
Review in Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- A Systematic Review of Parkinson's Disease Pharmacogenomics: Is There Time for Translation into the Clinics?International journal of molecular sciences · 2021Pooled it
- Parkinson's disease: pathogenesis and therapeutic strategies.Molecular biomedicine · 2026Review
- Article
- Organelle-Targeted Nanotherapeutics for Parkinson's Disease: From Pathogenesis to Preclinical Strategies and Translational Challenges.International journal of nanomedicine · 2026Review
- Bridging the gap in Parkinson's disease research: from general pathophysiology to advanced 3d cell culture models.Cell communication and signaling : CCS · 2025Review
- A genome-wide RNA interference screening reveals protectiveness of SNX5 knockdown in a Parkinson's disease cell model.Translational neurodegeneration · 2025Article
- The GBA1 K198E Variant Is Associated with Suppression of Glucocerebrosidase Activity, Autophagy Impairment, Oxidative Stress, Mitochondrial Damage, and Apoptosis in Skin Fibroblasts.International journal of molecular sciences · 2024Article
- FAM91A1-TBC1D23 complex structure reveals human genetic variations susceptible for PCH.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Regulation of Endosomal Trafficking by Rab7 and Its Effectors in Neurons: Clues from Charcot-Marie-Tooth 2B Disease.Biomolecules · 2023Review
- Abnormalities in Copper Status Associated with an Elevated Risk of Parkinson's Phenotype Development.Antioxidants (Basel, Switzerland) · 2023Review
- Genetic Evidence for Endolysosomal Dysfunction in Parkinson's Disease: A Critical Overview.International journal of molecular sciences · 2023Review
- Vacuolar protein sorting 35 (VPS35) acts as a tumor promoter via facilitating cell cycle progression in pancreatic ductal adenocarcinoma.Functional & integrative genomics · 2023Article
- CLEC16A interacts with retromer and TRIM27, and its loss impairs endosomal trafficking and neurodevelopment.Human genetics · 2023Article
- Review
- 'Fly-ing' from rare to common neurodegenerative disease mechanisms.Trends in genetics : TIG · 2022Review
- Retromer deficiency in Tauopathy models enhances the truncation and toxicity of Tau.Nature communications · 2022Article
- Article
- CROP: a retromer-PROPPIN complex mediating membrane fission in the endo-lysosomal system.The EMBO journal · 2022Article
- Monogenic Parkinson's Disease: Genotype, Phenotype, Pathophysiology, and Genetic Testing.Genes · 2022Review
- Dopaminergic Axons: Key Recitalists in Parkinson's Disease.Neurochemical research · 2022Review
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 1 institution in 1 country.
Funding
Abstract
Parkinson's Disease (PD) is a multi-system neurodegenerative disease where approximately 90% of cases are idiopathic. The remaining 10% of the cases can be traced to a genetic origin and research has largely focused on these associated genes to gain a better understanding of the molecular and cellular pathogenesis for PD. The gene encoding vacuolar protein sorting protein 35 (VPS35) has been definitively linked to late onset familial PD following the identification of a point mutation (D620N) as the causal agent in a Swiss family. Since its discovery, numerous studies have been undertaken to characterize the role of VPS35 in cellular processes and efforts have been directed toward understanding the perturbations caused by the D620N mutation. In this review, we examine what is currently known about VPS35, which has pleiotropic effects, as well as proposed mechanisms of pathogenesis by the D620N mutation. A brief survey of other VPS35 polymorphisms is also provided. Lastly, model systems that are being utilized for these investigations and possible directions for future research are discussed.
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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.