26 research outputs found
Targeting Huntington’s disease through histone deacetylases
Get PDFHuntington’s disease (HD) is a debilitating neurodegenerative condition with significant burdens on both patient and healthcare costs. Despite extensive research, treatment options for patients with this condition remain limited. Aberrant post-translational modification (PTM) of proteins is emerging as an important element in the pathogenesis of HD. These PTMs include acetylation, phosphorylation, methylation, sumoylation and ubiquitination. Several families of proteins are involved with the regulation of these PTMs. In this review, I discuss the current evidence linking aberrant PTMs and/or aberrant regulation of the cellular machinery regulating these PTMs to HD pathogenesis. Finally, I discuss the evidence suggesting that pharmacologically targeting one of these protein families the histone deacetylases may be of potential therapeutic benefit in the treatment of HD
Early or Late-Stage Anti-N-Terminal Huntingtin Intrabody Gene Therapy Reduces Pathological Features in B6.HDR6/1 Mice
No full textA Huntington's disease phenocopy characterized by pallido-nigro-luysian degeneration with brain iron accumulation and p62-positive glial inclusions
No full textMolecular analysis of Huntington's disease and linked polymorphisms in the Indian population
No full textHuntingtin gene CAG repeat numbers in Chinese patients with Huntington's disease and controls
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CAG repeat size in Huntingtin alleles is associated with cancer prognosis
No full textInternational audienc
Beyond the redox imbalance: Oxidative stress contributes to an impaired GLUT3 modulation in Huntington's disease
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