Evidence map›Paper›PMID 27619535›Full record

ReviewMovement disorders : official journal of the Movement Disorder Society2016

Endolysosomal dysfunction in Parkinson's disease: Recent developments and future challenges.

Lauren R Kett, William T Dauer

Abstract readReview
In one paragraph

Review in Movement disorders : official journal of the Movement Disorder Society, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Endosomal Acid-Base Homeostasis in Neurodegenerative Diseases.Reviews of physiology, biochemistry and pharmacology · 2023
    Article
  6. Review
  7. Review
  8. Article
  9. A Brain-Penetrant Stearoyl-CoA Desaturase Inhibitor Reverses α-Synuclein Toxicity.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Female Sex and Brain-Selective Estrogen Benefit α-Synuclein Tetramerization and the PD-like Motor Syndrome in 3K Transgenic Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    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

2 authors.

Lauren R KettDepartment of Neurology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
William T DauerDepartment of Neurology, University of Michigan Medical School, Ann Arbor, Michigan, USA. dauer@med.umich.edu.

Funding

MICHIGAN MEDICAL SCIENTIST TRAINING PROGRAMT32GM007863 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COLLINS, KATHLEEN L. · 1985 to 2024
$38.3M
Public Outreach and Education CoreP50NS091856 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ALBIN, ROGER L · 2014 to 2019
$10.1M
TorsinA function and dystonia-related dysfunction in developing and mature CNSR01NS077730 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DAUER, WILLIAM T. · 2013 to 2017
$1.9M
The Mechanism of LRRK2-Mediated Neurodegneration in Parkinson's DiseaseR01NS061098 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DAUER, WILLIAM T. · 2008 to 2010
$939k
The Role of Lysosomal Dysfunction in Parkinson Disease-Related NeurodegenerationF31NS078817 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KETT, LAUREN REBECCA · 2013 to 2013
$29k
NIGMS NIH HHS T32 GM007863NINDS NIH HHS F31 NS078817NINDS NIH HHS P50 NS091856NINDS NIH HHS R01 NS061098NINDS NIH HHS R01 NS077730
6 · The paper itself

Abstract

Increasingly, genetic, cell biological, and in vivo work emphasizes the role of the endolysosomal system dysfunction in Parkinson's disease pathogenesis. Yet many questions remain about the mechanisms by which primary endolysosomal dysfunction causes PD as well as how the endolysosomal system interacts with α-synuclein-mediated neurotoxicity. We recently described a new mouse model of parkinsonism in which loss of the endolysosomal protein Atp13a2 causes behavioral, neuropathological, and biochemical changes similar to those present in human subjects with ATP13A2 mutations. In this Scientific Perspectives, we revisit the evidence implicating the endolysosomal system in PD, current hypotheses of disease pathogenesis, and how recent studies refine these hypotheses and raise new questions for future research. © 2016 International Parkinson and Movement Disorder Society.

Indexed as

AnimalsHumansParkinson DiseaseProteinslysosomal proteinsProteinsAtp13a2endolysosomal systemKufor-Rakeb syndromeParkinson's disease

Identifiers

PMID27619535
PMCPMC5061051

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.