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Alleviating neurodegeneration in Drosophila models of PolyQ diseases

Polyglutamine (polyQ) diseases are a group of neurodegenerative conditions, induced from CAG trinucleotide repeat expansion within causative gene respectively. Generation of toxic proteins, containing polyQ-expanded tract, is the key process to cause neurodegeneration. Till now, although polyQ disea...

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Detalles Bibliográficos
Autores principales: Long, Zhe, Tang, Beisha, Jiang, Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4552282/
https://www.ncbi.nlm.nih.gov/pubmed/26331033
http://dx.doi.org/10.1186/2053-8871-1-9
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author Long, Zhe
Tang, Beisha
Jiang, Hong
author_facet Long, Zhe
Tang, Beisha
Jiang, Hong
author_sort Long, Zhe
collection PubMed
description Polyglutamine (polyQ) diseases are a group of neurodegenerative conditions, induced from CAG trinucleotide repeat expansion within causative gene respectively. Generation of toxic proteins, containing polyQ-expanded tract, is the key process to cause neurodegeneration. Till now, although polyQ diseases remain uncurable, numerous therapeutic strategies with great potential have been examined and have been proven to be effective against polyQ diseases, including diverse small biological molecules and many pharmacological compounds mainly through prevention on formation of aggregates and inclusions, acceleration on degradation of toxic proteins and regulation of cellular function. We review promising therapeutic strategies by using Drosophila models of polyQ diseases including HD, SCA1, SCA3 and SBMA.
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spelling pubmed-45522822015-09-01 Alleviating neurodegeneration in Drosophila models of PolyQ diseases Long, Zhe Tang, Beisha Jiang, Hong Cerebellum Ataxias Review Polyglutamine (polyQ) diseases are a group of neurodegenerative conditions, induced from CAG trinucleotide repeat expansion within causative gene respectively. Generation of toxic proteins, containing polyQ-expanded tract, is the key process to cause neurodegeneration. Till now, although polyQ diseases remain uncurable, numerous therapeutic strategies with great potential have been examined and have been proven to be effective against polyQ diseases, including diverse small biological molecules and many pharmacological compounds mainly through prevention on formation of aggregates and inclusions, acceleration on degradation of toxic proteins and regulation of cellular function. We review promising therapeutic strategies by using Drosophila models of polyQ diseases including HD, SCA1, SCA3 and SBMA. BioMed Central 2014-07-04 /pmc/articles/PMC4552282/ /pubmed/26331033 http://dx.doi.org/10.1186/2053-8871-1-9 Text en © Long et al.; licensee BioMed Central Ltd. 2014 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Review
Long, Zhe
Tang, Beisha
Jiang, Hong
Alleviating neurodegeneration in Drosophila models of PolyQ diseases
title Alleviating neurodegeneration in Drosophila models of PolyQ diseases
title_full Alleviating neurodegeneration in Drosophila models of PolyQ diseases
title_fullStr Alleviating neurodegeneration in Drosophila models of PolyQ diseases
title_full_unstemmed Alleviating neurodegeneration in Drosophila models of PolyQ diseases
title_short Alleviating neurodegeneration in Drosophila models of PolyQ diseases
title_sort alleviating neurodegeneration in drosophila models of polyq diseases
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4552282/
https://www.ncbi.nlm.nih.gov/pubmed/26331033
http://dx.doi.org/10.1186/2053-8871-1-9
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