Evidence map›Paper›PMID 24050397›Full record

ArticleNeuron2013

The function of α-synuclein.

Jacob T Bendor, Todd P Logan, Robert H Edwards

Registry-linked trialOpen access · bronzeAbstract readVideo-Audio Media
In one paragraph

Article in Neuron, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04405596 (Ambroxol as a Novel Disease Modifying Treatment for Lewy Body Dementia), which is not on this map. Cited by 446 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
446citing papers in PubMed, 3 pooled it
25.7field-weighted citation impact, top 1% 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.

NCT04405596 phase1 / phase2not yet recruitingnot on this mapstarted 2025, after this paper: background citation

Ambroxol as a Novel Disease Modifying Treatment for Lewy Body Dementia

TypeinterventionalSponsorLondon Health Sciences Centre Research Institute OR Lawson Research Institute of St. Joseph'sRan2025 to 2027Enrolled15ConditionsLewy Body DiseaseArmsAmbroxol Hydrochloride, Placebo
3 · Its place in the literature

Who cites it

446 citing papers in PubMed, 3 syntheses or guidelines pooled it, 851 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Cellular and systemic modifiers of alpha-synuclein proteostasis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Targeting ATScientific reports · 2026
    Article
  15. Roles in physiology and disease of the inositol phosphatase synaptojanin 1.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2026
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

386 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Jacob T BendorDepartments of Neurology and Physiology, Graduate Programs in Biomedical Sciences, Cell Biology and Neuroscience, UCSF School of Medicine, San Francisco, CA 94158-2517, USA.
Todd P Logan
Robert H Edwards
University of California, San Francisco · US

Funding

Alpha-Synuclein and the Synaptic Vesicle CycleR01NS062715 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI EDWARDS, ROBERT H · 2009 to 2014
$1.9M
NINDS NIH HHS NS062715NINDS NIH HHS R01 NS062715
6 · The paper itself

Abstract

Human genetics has indicated a causal role for the protein α-synuclein in the pathogenesis of familial Parkinson's disease (PD), and the aggregation of synuclein in essentially all patients with PD suggests a central role for this protein in the sporadic disorder. Indeed, the accumulation of misfolded α-synuclein now defines multiple forms of neural degeneration. Like many of the proteins that accumulate in other neurodegenerative disorders, however, the normal function of synuclein remains poorly understood. In this article, we review the role of synuclein at the nerve terminal and in membrane remodeling. We also consider the prion-like propagation of misfolded synuclein as a mechanism for the spread of degeneration through the neuraxis.

Indexed as

alpha-SynucleinAnimalsHumansNeurodegenerative DiseasesParkinson DiseasePrionsalpha-SynucleinPrions

Identifiers

PMID24050397
PMCPMC3866954
OpenAlexW2087482196

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

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 Socratic graph.