Emerging Therapies for Huntington’s Disease – Focus on N-Terminal Huntingtin and Huntingtin Exon 1
Author:
Publisher
Informa UK Limited
Subject
Pharmacology (medical),Gastroenterology,Oncology,Rheumatology,Immunology and Allergy
Reference163 articles.
1. Modeling Manifest Huntington’s Disease Prevalence Using Diagnosed Incidence and Survival Time
2. The Prevalence of Huntington's Disease
3. Length of Uninterrupted CAG, Independent of Polyglutamine Size, Results in Increased Somatic Instability, Hastening Onset of Huntington Disease
4. CAG Repeat Not Polyglutamine Length Determines Timing of Huntington’s Disease Onset
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1. Exploring molecular mechanisms, therapeutic strategies, and clinical manifestations of Huntington’s disease;Archives of Pharmacal Research;2024-05-19
2. AAV-Mediated CAG-Targeting Selectively Reduces Polyglutamine-Expanded Protein and Attenuates Disease Phenotypes in a Spinocerebellar Ataxia Mouse Model;International Journal of Molecular Sciences;2024-04-15
3. Huntington’s Disease: Complex Pathogenesis and Therapeutic Strategies;International Journal of Molecular Sciences;2024-03-29
4. Huntingtin HTT1a is generated in a CAG repeat-length-dependent manner in human tissues;Molecular Medicine;2024-03-08
5. Antisense oligonucleotide-mediated disruption of HTT caspase-6 cleavage site ameliorates the phenotype of YAC128 Huntington disease mice;Neurobiology of Disease;2024-01
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