Trinucleotide repeat length instability and age of onset in Huntington's disease

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Items 101–200 of 998

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11. Small-molecule ligand induces nucleotide flipping in (CAG)n trinucleotide repeats
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14. Trinucleotide repeat length and progression of illness in Huntington's disease.
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15. Laboratory Guidelines for Huntington Disease Genetic Testing
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16. The Emergence of Modern Neuroscience: Some Implications for Neurology and Psychiatry
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18. Therapeutic approaches to Huntington disease: from the bench to the clinic
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19. Interaction of normal and expanded CAG repeat sizes influences age at onset of Huntington disease
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24. The HTT CAG-Expansion Mutation Determines Age at Death but Not Disease Duration in Huntington Disease
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25. Microglial depletion prevents extracellular matrix changes and striatal volume reduction in a model of Huntington's disease
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27. Molecular Genetics of Huntington's Disease
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28. Trinucleotide repeat length and clinical progression in Huntington's disease
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29. Genetic modifiers of Huntington's disease
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30. Japanese Families with Autosomal Dominant Pure Cerebellar Ataxia Map to Chromosome 19p13.1-p13.2 and Are Strongly Associated with Mild CAG Expansions in the Spinocerebellar Ataxia Type 6 Gene in Chromosome 19p13.1
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31. A Genome Scan for Modifiers of Age at Onset in Huntington Disease: The HD MAPS Study
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32. The association of CAG repeat length with clinical progression in Huntington disease
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33. Motor abnormalities in premanifest persons with Huntington's disease: The PREDICT‐HD study
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34. Stoichiometry of Base Excision Repair Proteins Correlates with Increased Somatic CAG Instability in Striatum over Cerebellum in Huntington's Disease Transgenic Mice
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35. Role of oxidative DNA damage in mitochondrial dysfunction and Huntington’s disease pathogenesis
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36. Trinucleotide repeats in the human androgen receptor: a molecular basis for disease
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37. Mechanisms of Disease: histone modifications in Huntington's disease
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38. Mutational bias provides a model for the evolution of Huntington's disease and predicts a general increase in disease prevalence
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39. Reduced Penetrance of the Huntington's Disease Mutation
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40. The contribution of cis-elements to disease-associated repeat instability: clinical and experimental evidence
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41. Caspases and neurodegeneration: on the cutting edge of new therapeutic approaches
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42. DNA analysis in hereditary dentatorubral-pallidoluysian atrophy
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43. Features of trinucleotide repeat instability in vivo
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44. A role for autophagy in Huntington's disease
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45. Factors associated with HD CAG repeat instability in Huntington disease
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46. Implications of FRA16A Structure for the Mechanism of Chromosomal Fragile Site Genesis
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47. Huntington’s disease: Clinical presentation and treatment
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48. Polyglutamine domain flexibility mediates the proximity between flanking sequences in huntingtin
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49. Psychiatric and Cognitive Difficulties as Indicators of Juvenile Huntington Disease Onset in 29 Patients
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50. Patterns of CAG repeat instability in the central nervous system and periphery in Huntington’s disease and in spinocerebellar ataxia type 1
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51. Optineurin: A Coordinator of Membrane-Associated Cargo Trafficking and Autophagy
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52. Dopamine release is severely compromised in the R6/2 mouse model of Huntington's disease
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55. Neuropsychiatric Correlates and Treatment of Lenticulostriatal Diseases
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57. PGC-1alpha downstream transcription factors NRF-1 and TFAM are genetic modifiers of Huntington disease
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59. HD iPSC-derived neural progenitors accumulate in culture and are susceptible to BDNF withdrawal due to glutamate toxicity
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64. Current and Possible Future Therapeutic Options for Huntington’s Disease
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65. A majority of Huntington's disease patients may be treatable by individualized allele-specific RNA interference
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66. Iron dysregulation in Huntington's disease
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67. Nicotinamide improves motor deficits and upregulates PGC-1α and BDNF gene expression in a mouse model of Huntington's disease
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71. Timing and Impact of Psychiatric, Cognitive, and Motor Abnormalities in Huntington Disease
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75. Clinical correlation of striatal 1H MRS changes in Huntington’s disease
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77. Neuroinflammation in Neurodegenerative Disorders: Current Knowledge and Therapeutic Implications
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81. Human Huntington's disease iPSC-derived cortical neurons display altered transcriptomics, morphology, and maturation
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83. Precise Excision of the CAG Tract from the Huntingtin Gene by Cas9 Nickases
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88. Transgenic models of Huntington's disease
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89. A Brief History of Triplet Repeat Diseases
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90. Age at onset in Huntington’s disease is modified by the autophagy pathway: implication of the V471A polymorphism in Atg7
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95. DNA repeat expansions and human disease
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96. Environmental factors as modulators of neurodegeneration: Insights from gene–environment interactions in Huntington's disease
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97. Brain urea increase is an early Huntington’s disease pathogenic event observed in a prodromal transgenic sheep model and HD cases
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98. Functional decline in Huntington's disease
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