Evidence map›Paper›PMID 35588987›Full record

ReviewNeurobiology of disease2022

Understanding the contributions of VPS35 and the retromer in neurodegenerative disease.

Erin T Williams, Xi Chen, P Anthony Otero, Darren J Moore

Open access · goldAbstract readReview
In one paragraph

Review in Neurobiology of disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
6.1field-weighted citation impact, top 3% of its field
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

31 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Genetic and environmental risk factors of Parkinsonism.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Vacuolar protein sorting 35 regulates retinal neurovascular functionInternational journal of ophthalmology · 2026
    Article
  11. The Neuronal Golgi Network and Its Acolytes.Sub-cellular biochemistry · 2026
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. α-Synuclein: Multiple pathogenic roles in trafficking and proteostasis pathways in Parkinson's disease.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024
    Review
  19. Review
  20. Review
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 at 1 institution in 1 country.

Erin T WilliamsDepartment of Neurodegenerative Science, Van Andel Institute, Grand Rapids, MI 49503, USA.
Xi ChenDepartment of Neurodegenerative Science, Van Andel Institute, Grand Rapids, MI 49503, USA.
P Anthony OteroDepartment of Neurodegenerative Science, Van Andel Institute, Grand Rapids, MI 49503, USA.
Darren J MooreDepartment of Neurodegenerative Science, Van Andel Institute, Grand Rapids, MI 49503, USA. Electronic address: Darren.Moore@vai.org.
Van Andel Institute · US

Funding

Exploring mechanisms of Parkinson's disease-linked D620N VPS35 in rat modelsR01NS117137 · NINDS · VAN ANDEL RESEARCH INSTITUTE · PI MOORE, DARREN JOHN · 2020 to 2024
$2.2M
Mechanisms of VPS35-Dependent Neurodegeneration in Parkinson's DiseaseR01NS105432 · NINDS · VAN ANDEL RESEARCH INSTITUTE · PI MOORE, DARREN JOHN · 2017 to 2021
$2.1M
NINDS NIH HHS R01 NS105432NINDS NIH HHS R01 NS117137
6 · The paper itself

Abstract

Perturbations of the endolysosomal pathway have been suggested to play an important role in the pathogenesis of several neurodegenerative diseases, including Parkinson's disease (PD) and Alzheimer's disease (AD). Specifically, VPS35 and the retromer complex play an important role in the endolysosomal system and are implicated in the pathophysiology of these diseases. A single missense mutation in VPS35, Asp620Asn (D620N), is known to cause late-onset, autosomal dominant familial PD. In this review, we focus on the emerging role of the PD-linked D620N mutation in causing retromer dysfunction and dissect its implications in neurodegeneration. Additionally, we will discuss how VPS35 and the retromer are linked to AD, amyotrophic lateral sclerosis, and primary tauopathies. Interestingly, reduced levels of VPS35 and other retromer components have been observed in post-mortem brain tissue, suggesting a role for the retromer in the pathophysiology of these diseases. This review will provide a comprehensive dive into the mechanisms of VPS35 dysfunction in neurodegenerative diseases. Furthermore, we will highlight outstanding questions in the field and the retromer as a therapeutic target for neurodegenerative disease at large.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesParkinson DiseaseEndosomesHumansMutationVesicular Transport ProteinsVesicular Transport ProteinsVPS35 protein, humanAlzheimer's diseaseAmyotrophic lateral sclerosisAutophagyCargoEndosomeGolgiLRRK2LysosomeMitochondriaParkinson's diseaseRetromer complexTauTauopathiesVesicular sortingVPS35

Identifiers

PMID35588987
PMCPMC9233057
OpenAlexW4280546647

What OpenQuestion holds

Textmetadata
LicenceTDM
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.