Evidence map›Paper›PMID 36233303›Full record

ArticleInternational journal of molecular sciences2022

Saposin C, Key Regulator in the Alpha-Synuclein Degradation Mediated by Lysosome.

Clara Ruz, Francisco J Barrero, Javier Pelegrina, Sara Bandrés-Ciga, Francisco Vives, Raquel Duran

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Prosaposin in CNS health and disease, metabolic stress and exercise adaptation.Journal of molecular medicine (Berlin, Germany) · 2026
    Review
  3. Review
  4. A novel homozygousThe Journal of international medical research · 2024
    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

6 authors at 3 institutions in 2 countries.

Clara RuzDepartment of Physiology and Institute of Neurosciences "Federico Olóriz", Centre of Biomedical Research, University of Granada, 18016 Granada, Spain.ORCID 0000-0003-1846-3962
Francisco J BarreroInstituto de Investigación Biosanitaria ibs.GRANADA, 18012 Granada, Spain.ORCID 0000-0001-8490-2789
Javier PelegrinaMovement Disorders Unit, University Hospital Clinic San Cecilio, 18016 Granada, Spain.
Sara Bandrés-CigaInstituto de Investigación Biosanitaria ibs.GRANADA, 18012 Granada, Spain.
Francisco VivesDepartment of Physiology and Institute of Neurosciences "Federico Olóriz", Centre of Biomedical Research, University of Granada, 18016 Granada, Spain.
Raquel DuranDepartment of Physiology and Institute of Neurosciences "Federico Olóriz", Centre of Biomedical Research, University of Granada, 18016 Granada, Spain.ORCID 0000-0002-5749-8968
Universidad de Granada · ESInstituto de Investigación Biosanitaria de Granada · ESNational Institutes of Health · US

Funding

Fundación Progreso y Salud PI-0424-2014Regional Government of Andalusia B-CTS-702-UGR20
6 · The paper itself

Abstract

Lysosomal dysfunction has been proposed as one of the most important pathogenic molecular mechanisms in Parkinson disease (PD). The most significant evidence lies in the

Indexed as

alpha-SynucleinParkinson Diseasebeta-Galactosidasebeta-N-AcetylhexosaminidasesCathepsin DGlucosylceramidaseHexosaminidase BHumansLysosomesMutationSaposinsalpha-Synucleinbeta-Galactosidasebeta-N-AcetylhexosaminidasesCathepsin DGlucosylceramidaseHexosaminidase BSaposinsCathepsin Dlysosomal dysfunctionParkinson’s diseasePSAPβ-glucocerebrosidase

Identifiers

PMID36233303
PMCPMC9569857
OpenAlexW4303946054

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.