ArticleThe European journal of neuroscience2017
Modelling idiopathic Parkinson disease as a complex illness can inform incidence rate in healthy adults: the P
Article in The European journal of neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 26 citations in OpenAlex.
- Development of a simplified smell test to identify Parkinson's disease using multiple cohorts, machine learning and item response theory.NPJ Parkinson's disease · 2025Article
- Investigating the Effect of an Anti-Inflammatory Drug in Determining NURR1 Expression and Thus Exploring the Progression of Parkinson's Disease.Physiological research · 2024Article
- [Dihydromyricetin alleviates pyroptosis and necroptosis in mice with MPTP-induced chronic Parkinson's disease by inducing autophagy].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Evaluation of the PREDIGT score's performance in identifying newly diagnosed Parkinson's patients without motor examination.NPJ Parkinson's disease · 2022Article
- New Perspectives on Immune Involvement in Parkinson's Disease Pathogenesis.Journal of Parkinson's disease · 2022Review
- TLR2 and TLR4 in Parkinson's disease pathogenesis: the environment takes a toll on the gut.Translational neurodegeneration · 2021Review
- Alpha-synuclein research: defining strategic moves in the battle against Parkinson's disease.NPJ Parkinson's disease · 2021Review
- Therapy of Parkinson's Disease Subtypes.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Review
- Molecular evidence of impaired iron metabolism and its association with Parkinson's disease progression.3 Biotech · 2020Article
- Perspective: Current Pitfalls in the Search for Future Treatments and Prevention of Parkinson's Disease.Frontiers in neurology · 2020Review
- NADPH Oxidase Mediates Membrane Androgen Receptor-Induced Neurodegeneration.Endocrinology · 2019Article
- Dysregulated Lipid Metabolism and Its Role in α-Synucleinopathy in Parkinson's Disease.Frontiers in neuroscience · 2019Review
- Review
- Holocranohistochemistry enables the visualization of α-synuclein expression in the murine olfactory system and discovery of its systemic anti-microbial effects.Journal of neural transmission (Vienna, Austria : 1996) · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Fifty-five years after the concept of dopamine replacement therapy was introduced, Parkinson disease (PD) remains an incurable neurological disorder. To date, no disease-modifying therapeutic has been approved. The inability to predict PD incidence risk in healthy adults is seen as a limitation in drug development, because by the time of clinical diagnosis ≥ 60% of dopamine neurons have been lost. We have designed an incidence prediction model founded on the concept that the pathogenesis of PD is similar to that of many disorders observed in ageing humans, i.e. a complex, multifactorial disease. Our model considers five factors to determine cumulative incidence rates for PD in healthy adults: (i) DNA variants that alter susceptibility (D), e.g. carrying a LRRK2 or GBA risk allele; (ii) Exposure history to select environmental factors including xenobiotics (E); (iii) Gene-environment interactions that initiate pathological tissue responses (I), e.g. a rise in ROS levels, misprocessing of amyloidogenic proteins (foremost, α-synuclein) and dysregulated inflammation; (iv) sex (or gender; G); and importantly, (v) time (T) encompassing ageing-related changes, latency of illness and propagation of disease. We propose that cumulative incidence rates for PD (P
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.