Results 151 to 160 of about 9,196 (170)

B09 One antisense oligonucleotide as a potential therapy for polyglutamine disorders

Journal of Neurology, Neurosurgery & Psychiatry, 2010
Background To date there are nine known polyglutamine (polyQ) disorders: spinal bulbar muscular atrophy (SBMA), dentatorubral-pallidoluysian atrophy (DRPLA), Huntington9s disease (HD) and spinocerebellar ataxias (SCA1, 2, 3, 6, 7, and 17). These diseases are all caused by an expansion of CAG repeats in a gene that is translated into an expanded ...
W M C van Roon-Mom, M M Evers, J C T van Deutekom, S A M Mulders, A M Aartsma-Rus, J T den Dunnen, G-J B van Ommen   +6 more
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Calpains in the Molecular Pathogenesis of Polyglutamine Disorders and Their Potential as a Therapeutic Target

2017
Together with cancer and cardiovascular disorders, neurodegenerative diseases such as Alzheimer and Parkinson disease are an increasingly important medical issue for the aging society of the 21st century. Multiple factors such as environmental influences and individual living conditions act as important modulators of neuropathology.
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[Histone deacetylase inhibitors as therapeutic agents for polyglutamine disorders].

Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics, 2010
During the past few years, gene expression studies have shown that the perturbation of transcription frequently results in neuronal dysfunction in polyglutamine (PolyQ) diseases such as Huntington's disease (HD). Histone deacetylases (HDACs) act as repressors of transcription through interaction with co-repressor complexes, leading to chromatin ...
Hong, Jiang, Dandan, Jia, Beisha, Tang
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Genetic modeling of a neurodegenerative polyglutamine disorder in zebrafish and analysis of polyglutamine aggregate dynamics.

2012
Polyglutamine (polyQ) diseases are a family of nine neurodegenerative disorders caused by an unstable CAG expansion in the respective genes. One polyQ disease, spinocerebellar ataxia type 3 (SCA-3) disease was modeled by stable overexpression of pathogenic C-terminal Atx-3 in zebrafish Purkinje cells.
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Antisense oligonucleotide therapeutics in neurodegenerative diseases: the case of polyglutamine disorders

Brain, 2020
Ana C Silva, Sara M Lopes, Carina Henriques   +2 more
exaly  

Drosophila Models of Polyglutamine Disorders

2006
GEORGE R. JACKSON, TZU-KANG SANG, J. PAUL TAYLOR   +2 more
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The Molecular Basis of Huntington's Disease and Polyglutamine Disorders

Biochemical Society Transactions, 2000
Benn, C, Hay, D, Hockly, E, Gonitel, R, Lievens, J C, Mahal, Amarbirpal, Sathasivam, K, Spasic-Boskovic, O, Smith, D, Woodman, B, Bates, G   +10 more
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Mesenchymal stem cells for lysosomal storage and polyglutamine disorders: Possible shared mechanisms

European Journal of Clinical Investigation, 2022
Catarina Oliveira Miranda
exaly  

Developmental Alterations in Adult‐Onset Neurodegenerative Disorders: Lessons from Polyglutamine Diseases

Movement Disorders, 2021
Chandrakanth Reddy Edamakanti, Puneet Opal   +1 more
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Pathological mechanisms of polyglutamine disorder in Drosophila model of Huntington disease

2020
The first publication in my thesis surveyed the impacts of adenosine homeostasis and its underlying mechanisms in Huntington disease (HD) pathogenesis using a Drosophila model. In the second publication, we have extended the use of HD model flies to monitor mHTT effects on innate immune response.
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