ArticleInternational review of movement disorders2021
Mechanisms of
Article in International review of movement disorders, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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
12 citing papers in PubMed, 22 citations in OpenAlex.
- Parkinson's disease-linked D620N mutation selectively alters the brain-specific protein interactome of VPS35.Neurobiology of disease · 2026Article
- Parkinson's disease-linked D620N mutation selectively alters the brain-specific protein interactome of VPS35.bioRxiv : the preprint server for biology · 2026Article
- LRRK2 as a Potential Disease-Modifying Target in Sporadic Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2026Review
- Lipid metabolism in health and disease: Mechanistic and therapeutic insights for Parkinson's disease.Chinese medical journal · 2025Review
- Adaptive immunity in the pathogenesis and treatments of Parkinson's disease.NeuroImmune pharmacology and therapeutics · 2025Review
- VPS35 or retromer as a potential target for neurodegenerative disorders: barriers to progress.Expert opinion on therapeutic targets · 2024Review
- Intermittent hypoxia training enhances Aβ endocytosis by plaque associated microglia via VPS35-dependent TREM2 recycling in murine Alzheimer's disease.Alzheimer's research & therapy · 2024Article
- VPS35 and retromer dysfunction in Parkinson's disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Review
- Article
- VPS35 and α-Synuclein fail to interact to modulate neurodegeneration in rodent models of Parkinson's disease.Molecular neurodegeneration · 2023Article
- Understanding the contributions of VPS35 and the retromer in neurodegenerative disease.Neurobiology of disease · 2022Review
- Developmental pathways linked to the vulnerability of adult midbrain dopaminergic neurons to neurodegeneration.Frontiers in molecular neuroscience · 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 is a sporadic and common neurodegenerative movement disorder resulting from the complex interplay between genetic risk, aging and environmental exposure. Familial forms of PD account for ~10% of cases and are known to result from the inheritance of mutations in at least 15 genes. Mutations in the
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.