Evidence map›Paper›PMID 30717266›Full record

ReviewBrain sciences2019

Parkinsonisms and Glucocerebrosidase Deficiency: A Comprehensive Review for Molecular and Cellular Mechanism of Glucocerebrosidase Deficiency.

Emilia M Gatto, Gustavo Da Prat, Jose Luis Etcheverry, Guillermo Drelichman, Martin Cesarini

Open access · goldAbstract readReview
In one paragraph

Review in Brain sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

10 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Molecules (Basel, Switzerland) · 2020
    Article
  6. Article
  7. Fabry Disease With Concomitant Lewy Body Disease.Journal of neuropathology and experimental neurology · 2020
    Article
  8. Review
  9. Review
  10. Editorial forBrain sciences · 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

5 authors at 2 institutions in 1 country.

Emilia M GattoDepartment of Neurology, Parkinson's Disease and Movement Disorders Section, Institute of Neuroscience of Buenos Aires (INEBA). Guardia Vieja 4435, Buenos Aires C1192AAW, Argentina. emiliamgatto@gmail.com.
Gustavo Da PratDepartment of Neurology, Parkinson's Disease and Movement Disorders Section, Institute of Neuroscience of Buenos Aires (INEBA). Guardia Vieja 4435, Buenos Aires C1192AAW, Argentina. gustavoda_prat@hotmail.com.
Jose Luis EtcheverryDepartment of Neurology, Parkinson's Disease and Movement Disorders Section, Institute of Neuroscience of Buenos Aires (INEBA). Guardia Vieja 4435, Buenos Aires C1192AAW, Argentina. jletcheverry_1@yahoo.com.ar.
Guillermo DrelichmanHospital de Niños Ricardo Gutiérrez, Gallo 1330, Buenos Aires C1425EFD, Argentina. martisncesarini23@gmail.com.
Martin CesariniDepartment of Neurology, Parkinson's Disease and Movement Disorders Section, Institute of Neuroscience of Buenos Aires (INEBA). Guardia Vieja 4435, Buenos Aires C1192AAW, Argentina. martisncesarini23@gmail.com.
Instituto de Neurología de Buenos Aires · ARHospital General de Niños Ricardo Gutierrez · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the last years, lysosomal storage diseases appear as a bridge of knowledge between rare genetic inborn metabolic disorders and neurodegenerative diseases such as Parkinson's disease (PD) or frontotemporal dementia. Epidemiological studies helped promote research in the field that continues to improve our understanding of the link between mutations in the glucocerebrosidase (GBA) gene and PD. We conducted a review of this link, highlighting the association in GBA mutation carriers and in Gaucher disease type 1 patients (GD type 1). A comprehensive review of the literature from January 2008 to December 2018 was undertaken. Relevance findings include: (1) There is a bidirectional interaction between GBA and α- synuclein in protein homeostasis regulatory pathways involving the clearance of aggregated proteins. (2) The link between GBA deficiency and PD appears not to be restricted to α⁻synuclein aggregates but also involves Parkin and PINK1 mutations. (3) Other factors help explain this association, including early and later endosomes and the lysosomal-associated membrane protein 2A (LAMP-2A) involved in the chaperone-mediated autophagy (CMA). (4) The best knowledge allows researchers to explore new therapeutic pathways alongside substrate reduction or enzyme replacement therapies.

Indexed as

Gaucher diseaseglucocerebrosidaseParkinson’s disease

Identifiers

PMID30717266
PMCPMC6406566
OpenAlexW2913305529

What OpenQuestion 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 OpenQuestion graph.