Evidence map›Paper›PMID 25960916›Full record

ReviewParkinson's disease2015

Neurophysiology of Drosophila models of Parkinson's disease.

Ryan J H West, Rebecca Furmston, Charles A C Williams, Christopher J H Elliott

Abstract readReview
In one paragraph

Review in Parkinson's disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed.

  1. Medical science pulse · 2025
    Article
  2. Reduced penetrance of Parkinson's disease models.Medizinische Genetik : Mitteilungsblatt des Berufsverbandes Medizinische Genetik e.V · 2022
    Article
  3. Article
  4. Observational
  5. Article
  6. Article
  7. G3 (Bethesda, Md.) · 2020
    Article
  8. Review
  9. Vitamin BCell research · 2019
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Dopamine Modulates Serotonin Innervation in theFrontiers in systems neuroscience · 2017
    Article
  17. Circuit Analysis of a Drosophila Dopamine Type 2 Receptor That Supports Anesthesia-Resistant Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Ryan J H WestDepartment of Biology, University of York, York YO1 5DD, UK.
Rebecca FurmstonDepartment of Biology, University of York, York YO1 5DD, UK.
Charles A C WilliamsDepartment of Biology, University of York, York YO1 5DD, UK ; The MRC Protein Phosphorylation and Ubiquitylation Unit, The Sir James Black Centre, College of Life Sciences, University of Dundee, Dow Street, Dundee DD1 5EH, UK.
Christopher J H ElliottDepartment of Biology, University of York, York YO1 5DD, UK.

Funding

Parkinson's UK H-1201Wellcome Trust
6 · The paper itself

Abstract

We provide an insight into the role Drosophila has played in elucidating neurophysiological perturbations associated with Parkinson's disease- (PD-) related genes. Synaptic signalling deficits are observed in motor, central, and sensory systems. Given the neurological impact of disease causing mutations within these same genes in humans the phenotypes observed in fly are of significant interest. As such we observe four unique opportunities provided by fly nervous system models of Parkinson's disease. Firstly, Drosophila models are instrumental in exploring the mechanisms of neurodegeneration, with several PD-related mutations eliciting related phenotypes including sensitivity to energy supply and vesicular deformities. These are leading to the identification of plausible cellular mechanisms, which may be specific to (dopaminergic) neurons and synapses rather than general cellular phenotypes. Secondly, models show noncell autonomous signalling within the nervous system, offering the opportunity to develop our understanding of the way pathogenic signalling propagates, resembling Braak's scheme of spreading pathology in PD. Thirdly, the models link physiological deficits to changes in synaptic structure. While the structure-function relationship is complex, the genetic tractability of Drosophila offers the chance to separate fundamental changes from downstream consequences. Finally, the strong neuronal phenotypes permit relevant first in vivo drug testing.

Identifiers

PMID25960916
PMCPMC4414211

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Registered trials

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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.