Evidence map›Paper›PMID 21153060›Full record

ReviewMolecular neurobiology2011

Huntington's disease and Group I metabotropic glutamate receptors.

Fabiola M Ribeiro, Rita G W Pires, Stephen S G Ferguson

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
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  7. Review
  8. Noninvasive Relative Quantification of [Frontiers in neurology · 2018
    Article
  9. Article
  10. Article
  11. Sustained Gq-Protein Signaling Disrupts Striatal Circuits via JNK.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  12. Selective expression of mutant huntingtin during development recapitulates characteristic features of Huntington's disease.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  13. Article
  14. Article
  15. The function of metabotropic glutamate receptors in thalamus and cortex.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2014
    Review
  16. Article
  17. Article
  18. Article
  19. Article
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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

3 authors at 3 institutions in 2 countries.

Fabiola M RibeiroDepartamento de Bioquimica e Imunologia, ICB, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Rita G W Pires
Stephen S G Ferguson
Universidade Federal de Minas Gerais · BRUniversidade Federal do Espírito Santo · BRWestern University · CA

Funding

Canadian Institutes of Health Research MA-15506
6 · The paper itself

Abstract

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder characterized by involuntary body movement, cognitive impairment and psychiatric disturbance. A polyglutamine expansion in the amino-terminal region of the huntingtin (htt) protein is the genetic cause of HD. Htt protein interacts with a wide variety of proteins, and htt mutation causes cell signaling alterations in various neurotransmitter systems, including dopaminergic, glutamatergic, and cannabinoid systems, as well as trophic factor systems. This review will overview recent findings concerning htt-promoted alterations in cell signaling that involve different neurotransmitters and trophic factor systems, especially involving mGluR1/5, as glutamate plays a crucial role in neuronal cell death. The neuronal cell death that takes place in the striatum and cortex of HD patients is the most important factor underlying HD progression. Metabotropic glutamate receptors (mGluR1 and mGluR5) have a very controversial role in neuronal cell death and it is not clear whether mGluR1/5 activation either protects or exacerbates neuronal death. Thus, understanding how mutant htt protein affects glutamatergic receptor signaling will be essential to further establish a role for glutamate receptors in HD and develop therapeutic strategies to treat HD.

Indexed as

AnimalsCannabinoid Receptor ModulatorsCell SurvivalGlutamic AcidHumansHuntingtin ProteinHuntington DiseaseMutationNerve Tissue ProteinsNeuronsNuclear ProteinsPeptidesReceptors, Metabotropic GlutamateReceptors, N-Methyl-D-AspartateSignal TransductionCannabinoid Receptor ModulatorsGlutamic AcidHTT protein, humanHuntingtin ProteinNerve Tissue ProteinsNuclear ProteinsPeptidespolyglutamineReceptors, Metabotropic GlutamateReceptors, N-Methyl-D-Aspartate

Identifiers

PMID21153060
OpenAlexW2065034911

What OpenQuestion holds

Textmetadata
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.