Evidence map›Paper›PMID 39273169›Full record

ArticleInternational journal of molecular sciences2024

The GBA1 K198E Variant Is Associated with Suppression of Glucocerebrosidase Activity, Autophagy Impairment, Oxidative Stress, Mitochondrial Damage, and Apoptosis in Skin Fibroblasts.

Laura Patricia Perez-Abshana, Miguel Mendivil-Perez, Marlene Jimenez-Del-Rio, Carlos Velez-Pardo

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. 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.

Laura Patricia Perez-AbshanaNeuroscience Research Group, University of Antioquia, University Research Headquarters, Calle 62#52-59, Building 1, Laboratory 411/412, Medellin 050010, Colombia.
Miguel Mendivil-PerezNeuroscience Research Group, University of Antioquia, University Research Headquarters, Calle 62#52-59, Building 1, Laboratory 411/412, Medellin 050010, Colombia.ORCID 0000-0002-8824-379X
Marlene Jimenez-Del-RioNeuroscience Research Group, University of Antioquia, University Research Headquarters, Calle 62#52-59, Building 1, Laboratory 411/412, Medellin 050010, Colombia.ORCID 0000-0003-3477-2386
Carlos Velez-PardoNeuroscience Research Group, University of Antioquia, University Research Headquarters, Calle 62#52-59, Building 1, Laboratory 411/412, Medellin 050010, Colombia.ORCID 0000-0002-0557-0411

Funding

MinCiencias 1115-844-67799
6 · The paper itself

Abstract

Parkinson's disease (PD) is a multifactorial, chronic, and progressive neurodegenerative disorder inducing movement alterations as a result of the loss of dopaminergic (DAergic) neurons of the pars compacta in the substantia nigra and protein aggregates of alpha synuclein (α-Syn). Although its etiopathology agent has not yet been clearly established, environmental and genetic factors have been suggested as the major contributors to the disease. Mutations in the glucosidase beta acid 1 (

Indexed as

ApoptosisAutophagyFibroblastsGlucosylceramidaseMitochondriaOxidative Stressalpha-SynucleinHumansLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LysosomesMutationParkinson DiseaseSkinalpha-SynucleinGBA protein, humanGlucosylceramidaseLeucine-Rich Repeat Serine-Threonine Protein Kinase-2alpha-synucleinapoptosisautophagyglucocerebrosidaseK198E variantLRRK2Parkinsonskin fibroblast

Identifiers

PMID39273169
PMCPMC11394901

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.