ReviewHuman molecular genetics2015
Pathways to Parkinsonism Redux: convergent pathobiological mechanisms in genetics of Parkinson's disease.
Review in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses 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
60 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Cutaneous α-Synuclein and Age Spots in Neurodegeneration: A Systematic Review and Testable Hypothesis.International journal of molecular sciences · 2025Pooled it
- The SH-SY5Y cell line in Parkinson's disease research: a systematic review.Molecular neurodegeneration · 2017Pooled it
- Glycoprotein Non-Metastatic Melanoma Protein B (GPNMB): A Translational Pharmacodynamic Biomarker for PIKfyve Inhibition With VRG50635.Clinical and translational science · 2026Trial
- Simvastatin as a Potential Disease-Modifying Therapy for Patients with Parkinson's Disease: Rationale for Clinical Trial, and Current Progress.Journal of Parkinson's disease · 2017Trial
- ATP13A2 Loss of Function-Driven Polyamine Dysregulation Induces SAM Depletion and Epigenetic Astrocyte Toxicity.bioRxiv : the preprint server for biology · 2026Article
- Plasticity-Induced Motor Recovery of Bilateral Intermittent Theta Burst Stimulation in Parkinson's Disease: A Randomized, Double-Blind, Sham-Controlled, Crossover Trial.Neurology and therapy · 2026Article
- Parkinson's Disease: The Epidemiology, Risk Factors, Molecular Pathogenesis, Prevention, and Therapy.MedComm · 2025Review
- Burden of Parkinson's disease in Iran: disparities, trends, and the impact of social development indicators.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- CSF GPNMB in Parkinson's disease: A potential association with age and microglial activation.Journal of Parkinson's disease · 2024Article
- Interplay between α-synuclein and parkin genes: Insights of Parkinson's disease.Molecular biology reports · 2024Review
- DNA Damage and Parkinson's Disease.International journal of molecular sciences · 2024Review
- VPS35 and retromer dysfunction in Parkinson's disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Review
- Disruption of lysosomal proteolysis in astrocytes facilitates midbrain organoid proteostasis failure in an early-onset Parkinson's disease model.Nature communications · 2024Article
- Progranulin and GPNMB: interactions in endo-lysosome function and inflammation in neurodegenerative disease.Journal of neuroinflammation · 2023Review
- Shared molecular genetic factors influence subcortical brain morphometry and Parkinson's disease risk.NPJ Parkinson's disease · 2023Article
- Sex, Age, and Regional Differences inCurrent neuropharmacology · 2023Article
- Supramolecular organizing centers at the interface of inflammation and neurodegeneration.Frontiers in immunology · 2022Review
- Regional brain iron and gene expression provide insights into neurodegeneration in Parkinson's disease.Brain : a journal of neurology · 2021Article
- BrainCells · 2021Article
- Shared genetic etiology between Parkinson's disease and blood levels of specific lipids.NPJ Parkinson's disease · 2021Article
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.
Funding
Abstract
In the past few years, there have been a large number of genes identified that contribute to the lifetime risk of Parkinson's disease (PD). Some genes follow a Mendelian inheritance pattern, but others are risk factors for apparently sporadic PD. Here, we will focus on those genes nominated by genome-wide association studies (GWAS) in sporadic PD, with a particular emphasis on genes that overlap between familial and sporadic disease such as those encoding a-synuclein (SNCA), tau (MAPT), and leucine-rich repeat kinase 2 (LRRK2). We will advance the view that there are likely relationships between these genes that map not only to neuronal processes, but also to neuroinflammation. We will particularly discuss evidence for a role of PD proteins in microglial activation and regulation of the autophagy-lysosome system that is dependent on microtubule transport in neurons. Thus, there are at least two non-mutually exclusive pathways that include both non-cell-autonomous and cell-autonomous mechanisms in the PD brain. Collectively, these data have highlighted the amount of progress made in understanding PD and suggest ways forward to further dissect this disorder.
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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.