Evidence map›Paper›PMID 33671313›Full record

ReviewCells2021

Zebrafish Models of Autosomal Dominant Ataxias.

Ana Quelle-Regaldie, Daniel Sobrido-Cameán, Antón Barreiro-Iglesias, María Jesús Sobrido, Laura Sánchez

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Severe neurometabolic phenotype inFrontiers in molecular neuroscience · 2023
    Article
  6. Towards Zebrafish Models of CNS Channelopathies.International journal of molecular sciences · 2022
    Review
  7. ABiomedicines · 2022
    Article
  8. Review
  9. Structural Analysis and Spatiotemporal Expression ofInternational journal of molecular sciences · 2021
    Article
  10. Article
  11. 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

5 authors at 2 institutions in 1 country.

Ana Quelle-RegaldieDepartment of Zoology, Genetics and Physical Anthropology, Faculty of Veterinary Science, Universidade of Santiago de Compostela, 27002 Lugo, Spain.ORCID 0000-0003-0498-8741
Daniel Sobrido-CameánDepartment of Functional Biology, CIBUS, Faculty of Biology, Universidade de Santiago de Compostela, 15782 Santiago de Compostela, Spain.ORCID 0000-0001-8239-2965
Antón Barreiro-IglesiasDepartment of Functional Biology, CIBUS, Faculty of Biology, Universidade de Santiago de Compostela, 15782 Santiago de Compostela, Spain.ORCID 0000-0002-7507-080X
María Jesús SobridoInstituto de Investigación Biomédica de A Coruña (INIBIC), Servicio Galego de Saúde, 15006 Coruña, Spain.
Laura SánchezDepartment of Zoology, Genetics and Physical Anthropology, Faculty of Veterinary Science, Universidade of Santiago de Compostela, 27002 Lugo, Spain.ORCID 0000-0001-7927-5303
Universidade de Santiago de Compostela · ESInstituto de Investigación Biomédica de A Coruña · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hereditary dominant ataxias are a heterogeneous group of neurodegenerative conditions causing cerebellar dysfunction and characterized by progressive motor incoordination. Despite many efforts put into the study of these diseases, there are no effective treatments yet. Zebrafish models are widely used to characterize neuronal disorders due to its conserved vertebrate genetics that easily support genetic edition and their optic transparency that allows observing the intact CNS and its connections. In addition, its small size and external fertilization help to develop high throughput assays of candidate drugs. Here, we discuss the contributions of zebrafish models to the study of dominant ataxias defining phenotypes, genetic function, behavior and possible treatments. In addition, we review the zebrafish models created for X-linked repeat expansion diseases X-fragile/fragile-X tremor ataxia. Most of the models reviewed here presented neuronal damage and locomotor deficits. However, there is a generalized lack of zebrafish adult heterozygous models and there are no knock-in zebrafish models available for these diseases. The models created for dominant ataxias helped to elucidate gene function and mechanisms that cause neuronal damage. In the future, the application of new genetic edition techniques would help to develop more accurate zebrafish models of dominant ataxias.

Indexed as

AtaxiaDisease Models, AnimalSpinocerebellar DegenerationsZebrafishAnimalsHumansPhenotypeexpanded repeatsgenetic editionhereditary dominant ataxiasneurodegenerative disordersspinocerebellar ataxiasX-fragilezebrafish

Identifiers

PMID33671313
PMCPMC7922657
OpenAlexW3132734562

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.