Evidence map›Paper›PMID 20869586›Full record

ArticleNeuron2010

PolyQ disease: too many Qs, too much function?

Ian H Kratter, Steven Finkbeiner

Abstract readComment
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuron, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

  1. Article
  2. PolyQ-Expansion of Ataxin-2 Disrupts Microtubule Stability and Impairs Axon Outgrowth.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  3. Article
  4. Review
  5. The polyG diseases: a new disease entity.Acta neuropathologica communications · 2022
    Review
  6. Review
  7. Genetics, Mechanisms, and Therapeutic Progress in Polyglutamine Spinocerebellar Ataxias.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    Review
  8. Review
  9. Review
  10. Polyglutamine androgen receptor-mediated neuromuscular disease.Cellular and molecular life sciences : CMLS · 2016
    Review
  11. Article
  12. Article
  13. Article
  14. Modeling Huntington's disease with induced pluripotent stem cells.Molecular and cellular neurosciences · 2013
    Review
  15. Review
  16. Review
  17. Article
  18. Background-dependent effects of polyglutamine variation in the Arabidopsis thaliana gene ELF3.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  19. Review
  20. Pathogenic polyglutamine proteins cause dendrite defects associated with specific actin cytoskeletal alterations in Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Ian H KratterGladstone Institute of Neurological Disease, University of California, San Francisco, CA 94158, USA.
Steven Finkbeiner

Funding

Polyglutamine Conformation and NeurodegenerationR01NS045191 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI FINKBEINER, STEVEN M · 2003 to 2013
$4.4M
NINDS NIH HHS R01 NS045191
6 · The paper itself

Abstract

The nature of the gain-of-function toxicity found in polyglutamine (polyQ) diseases has been the subject of considerable debate. In this issue of Neuron, Duvick et al. and Nedelsky et al. show that, in two of these diseases, pathology is mediated by normal protein activity.

Identifiers

PMID20869586
PMCPMC3989162

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Registered trials

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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.