Evidence map›Paper›PMID 37637775›Full record

ArticleOxford open neuroscience2023

A Critical Review of Zebrafish Neurological Disease Models-2. Application: Functional and Neuroanatomical Phenotyping Strategies and Chemical Screens.

Edward A Burton, Harold A Burgess

Abstract read
In one paragraph

Article in Oxford open neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Evolution and development of extraocular motor neurons, nerves and muscles in vertebrates.Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft · 2024
    Review
  9. Review
  10. Article
  11. Article
  12. 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

2 authors.

Edward A BurtonPittsburgh Institute of Neurodegenerative Diseases, University of Pittsburgh, Pittsburgh, PA 15260, USA.ORCID 0000-0002-8072-4636
Harold A BurgessDivision of Developmental Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892, USA.ORCID 0000-0003-1966-7801

Funding

Pathogenic mechanisms of gene-environment interactions in Parkinson's diseaseR01ES022644 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BURTON, EDWARD ALAN · 2014 to 2018
$1.7M
ROS driven mitochondrial-telomere dysfunction during environmental stressR33ES025606 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI OPRESKO, PATRICIA L, VAN HOUTEN, BENNETT · 2017 to 2019
$1.6M
A Phenotype-Optimized Zebrafish Model of Progressive Supranuclear PalsyR33NS125280 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BURTON, EDWARD ALAN, SCHOPPIK, DAVID · 2023 to 2024
$531k
A Phenotype-Optimized Zebrafish Model of Progressive Supranuclear PalsyR61NS125280 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BURTON, EDWARD ALAN, SCHOPPIK, DAVID · 2022 to 2022
$497k
Functional evaluation of genes adjacent to risk-modulating SNPs in the pathogenesis of PSPR21NS123211 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BURTON, EDWARD ALAN · 2021 to 2021
$434k
Development of Zebrafish Taupoathy Models for Translational ResearchR21NS080881 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BURTON, EDWARD ALAN · 2013 to 2014
$419k
ROS driven mitochondrial-telomere dysfunction during environmental stressR21ES025606 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI OPRESKO, PATRICIA L, VAN HOUTEN, BENNETT · 2015 to 2016
$414k
Role of BET proteins in neuroinflammation in tauopathyI01BX003168 · VA · VETERANS HEALTH ADMINISTRATION · PI Edward Alan Burton · 2017 to 2026
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BLRD VA I01 BX003168NIEHS NIH HHS R01 ES022644NIEHS NIH HHS R21 ES025606NIEHS NIH HHS R33 ES025606NINDS NIH HHS R21 NS080881NINDS NIH HHS R21 NS123211NINDS NIH HHS R33 NS125280NINDS NIH HHS R61 NS125280
6 · The paper itself

Abstract

Extensive phylogenetic conservation of molecular pathways and neuroanatomical structures, associated with efficient methods for genetic modification, have been exploited increasingly to generate zebrafish models of human disease. A range of powerful approaches can be deployed to analyze these models with the ultimate goal of elucidating pathogenic mechanisms and accelerating efforts to find effective treatments. Unbiased neurobehavioral assays can provide readouts that parallel clinical abnormalities found in patients, although some of the most useful assays quantify responses that are not routinely evaluated clinically, and differences between zebrafish and human brains preclude expression of the full range of neurobehavioral abnormalities seen in disease. Imaging approaches that use fluorescent reporters and standardized brain atlases coupled with quantitative measurements of brain structure offer an unbiased means to link experimental manipulations to changes in neural architecture. Together, quantitative structural and functional analyses allow dissection of the cellular and physiological basis underlying neurological phenotypes. These approaches can be used as outputs in chemical modifier screens, which provide a major opportunity to exploit zebrafish models to identify small molecule modulators of pathophysiology that may be informative for understanding disease mechanisms and possible therapeutic approaches.

Indexed as

behaviorbrain imagingchemical screensdisease modelsneurological disorderszebrafish

Identifiers

PMID37637775
PMCPMC10455049

What OpenQuestion holds

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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.