ReviewNPJ Parkinson's disease2022
Redefining the hypotheses driving Parkinson's diseases research.
Review in NPJ Parkinson's disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 26 citations in OpenAlex.
- A new paradigm in Parkinson's disease: kidney-origin α-synuclein pathology driven by PKC signaling and aurothioglucose.Inflammopharmacology · 2026Review
- Early Prediction of Parkinson's Disease Progression by Integrating Research Cohort and Real-World Data Using Knowledge-Anchored Graph Learning.medRxiv : the preprint server for health sciences · 2026Article
- BullFish: Software for an automated stepwise analysis of positional and postural kinematics of zebrafish locomotion.iScience · 2026Article
- Molecular profiling of alpha-synuclein pathology and seeding activity in Parkinson's disease.Acta neuropathologica · 2026Article
- ZPT01, a herbal formula of Zingiberis Rhizoma, Paeoniae Radix and Tribuli Fructus, protects dopaminergic neurons and suppresses neuroinflammation in a Parkinson's disease model.Molecular biology reports · 2026Article
- Data-driven subtyping of early Parkinson's disease via mutual cross-attention fusion of EEG and dual-task gait features.NPJ Parkinson's disease · 2026Article
- There is not one Parkinson's disease, nor is there one cure.NPJ Parkinson's disease · 2025Article
- Neurodegeneration as Ecosystem Failure: A New Paradigm for Prevention and Treatment.International journal of molecular sciences · 2025Review
- Article
- Therapeutic Mechanisms of Exercise in Parkinson's Disease.International journal of molecular sciences · 2025Review
- From blood vessels to brain cells: Connecting the circulatory system and Parkinson's disease.Journal of Parkinson's disease · 2025Review
- Enhancements in Parkinson's Disease Management: Leveraging Levodopa Optimization and Surgical Breakthroughs.Current drug targets · 2025Review
- Scrutinizing neurodegenerative diseases: decoding the complex genetic architectures through a multi-omics lens.Human genomics · 2024Review
- Cohort-specific boolean models highlight different regulatory modules during Parkinson's disease progression.iScience · 2024Article
- Identification of Parkinson's disease PACE subtypes and repurposing treatments through integrative analyses of multimodal data.NPJ digital medicine · 2024Article
- How Lifetime Evolution of Parkinson's Disease Could Shape Clinical Trial Design: A Shared Patient-Clinician Viewpoint.Brain sciences · 2024Article
- Therapeutics for neurodegenerative diseases by targeting the gut microbiome: from bench to bedside.Translational neurodegeneration · 2024Review
- Different pieces of the same puzzle: a multifaceted perspective on the complex biological basis of Parkinson's disease.NPJ Parkinson's disease · 2023Review
- PARK7/DJ-1 in microglia: implications in Parkinson's disease and relevance as a therapeutic target.Journal of neuroinflammation · 2023Review
- Alpha Synuclein: Neurodegeneration and Inflammation.International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 3 countries.
Funding
Abstract
Parkinson's disease (PD) research has largely focused on the disease as a single entity centred on the development of neuronal pathology within the central nervous system. However, there is growing recognition that PD is not a single entity but instead reflects multiple diseases, in which different combinations of environmental, genetic and potential comorbid factors interact to direct individual disease trajectories. Moreover, an increasing body of recent research implicates peripheral tissues and non-neuronal cell types in the development of PD. These observations are consistent with the hypothesis that the initial causative changes for PD development need not occur in the central nervous system. Here, we discuss how the use of neuronal pathology as a shared, qualitative phenotype minimises insights into the possibility of multiple origins and aetiologies of PD. Furthermore, we discuss how considering PD as a single entity potentially impairs our understanding of the causative molecular mechanisms, approaches for patient stratification, identification of biomarkers, and the development of therapeutic approaches to PD. The clear consequence of there being distinct diseases that collectively form PD, is that there is no single biomarker or treatment for PD development or progression. We propose that diagnosis should shift away from the clinical definitions, towards biologically defined diseases that collectively form PD, to enable informative patient stratification. N-of-one type, clinical designs offer an unbiased, and agnostic approach to re-defining PD in terms of a group of many individual diseases.
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.