ReviewNeuroscience bulletin2010
Current understanding on the pathogenesis of polyglutamine diseases.
Review in Neuroscience bulletin, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Polyglutamine (PolyQ) Diseases: Navigating the Landscape of Neurodegeneration.ACS chemical neuroscience · 2024Review
- The interplay between oxidative stress and autophagy: focus on the development of neurological diseases.Behavioral and brain functions : BBF · 2022Review
- The emerging roles of long non-coding RNAs in polyglutamine diseases.Journal of cellular and molecular medicine · 2021Review
- New Synthetic 3-Benzoyl-5-Hydroxy-2Oxidative medicine and cellular longevity · 2020Article
- Article
- The Emerging Role of microRNAs in Polyglutamine Diseases.Frontiers in molecular neuroscience · 2019Article
- Enhanced molecular mobility of ordinarily structured regions drives polyglutamine disease.The Journal of biological chemistry · 2015Article
- Neuropathological staging of spinocerebellar ataxia type 2 by semiquantitative 1C2-positive neuron typing. Nuclear translocation of cytoplasmic 1C2 underlies disease progression of spinocerebellar ataxia type 2.Brain pathology (Zurich, Switzerland) · 2014Article
- A tale of a tail: Structural insights into the conformational properties of the polyglutamine protein ataxin-3.International journal of mass spectrometry · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polyglutamine (polyQ) diseases are a family of neurodegenerative disorders including Huntington's disease, spinobulbar muscular atrophy, dentatorubral-pallidoluysian atrophy and several spinocerebellar ataxias. polyQ diseases are caused by abnormal expansion of CAG repeats in certain genes. The expanded CAG repeats are then translated into a series of abnormally expanded polyQ tracts. Such polyQ tracts may induce misfolding of the disease-causing proteins. The present review mainly focuses on the common characteristics of the pathogenesis of these polyQ diseases, including conformational transition of proteins and its influence on the function of these proteins, the correlation between decreased ability of proteolysis and late-onset polyQ diseases, and the relationship between wide expression of disease-causing proteins and selective neuronal death.
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What OpenQuestion holds
Registered trials
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.