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Neurology, ISSN 0028-3878, 03/2012, Volume 78, Issue 10, pp. 690 - 695
Objective: Age at onset of diagnostic motor manifestations in Huntington disease (HD) is strongly correlated with an expanded CAG trinucleotide repeat. The... 
HOMOZYGOSITY | ALLELE | OF-ONSET | GENE | LENGTH | MUTATION | CHROMOSOMES | CLINICAL NEUROLOGY | TRINUCLEOTIDE REPEAT | Humans | Age of Onset | Alleles | Huntington Disease - genetics | Adult | Female | Genotype | Huntington Disease - diagnosis | Male | Trinucleotide Repeat Expansion | 164
Journal Article
European Journal of Nuclear Medicine and Molecular Imaging, ISSN 1619-7070, 06/2012, Volume 39, Issue 6, pp. 1030 - 1036
Purpose: To test in a longitudinal follow-up study whether basal glucose metabolism in subjects with a genetic risk of Huntington disease (HD) may influence... 
Neuroimaging | Brain | Nuclear medicine | Polyglutamine | Multiple regression analysis | Trinucleotide repeats | Regression analysis | Huntington's disease | trinucleotide repeat diseases | Glucose metabolism | Models | Mutation | Positron emission tomography | Age
Journal Article
European Journal of Nuclear Medicine and Molecular Imaging, ISSN 1619-7070, 06/2012, Volume 39, Issue 6, p. 1030
To test in a longitudinal follow-up study whether basal glucose metabolism in subjects with a genetic risk of Huntington disease (HD) may influence the onset... 
Glucose metabolism | Pets | Huntington's chorea | Genetic aspects | Diagnostic imaging | Glucose | Dextrose
Journal Article
Nature, ISSN 0028-0836, 05/2017, Volume 545, Issue 7652, pp. 108 - 111
Nine neurodegenerative diseases are caused by expanded polyglutamine (polyQ) tracts in different proteins, such as huntingtin in Huntington's disease and... 
PATHOGENESIS | CELLS | PROTEIN | MULTIDISCIPLINARY SCIENCES | MACHADO-JOSEPH-DISEASE | MUTANT HUNTINGTIN | ATAXIN-3 | INTRANUCLEAR INCLUSIONS | LC3 | MOUSE MODELS | AGGREGATION | Humans | Ubiquitin - metabolism | Male | Neurons - cytology | Autophagy | Brain - metabolism | Peptides - metabolism | Protein Domains | Ataxin-3 - chemistry | Female | Food Deprivation | Neurons - metabolism | Protein Stability | Ataxin-3 - metabolism | Disease Models, Animal | Binding, Competitive | Cell Line | Ataxin-3 - deficiency | Huntingtin Protein - metabolism | Mice, Inbred C57BL | Phagosomes - metabolism | Cells, Cultured | Mutant Proteins - genetics | Exons - genetics | Mutant Proteins - metabolism | Huntington Disease - metabolism | Huntingtin Protein - chemistry | Animals | Mutant Proteins - chemistry | Brain - pathology | Huntington Disease - genetics | Protein Binding | Mice | Huntingtin Protein - genetics | Mutation | Proteasome Endopeptidase Complex - metabolism | Beclin-1 - metabolism | Ataxin-3 - genetics | Physiological aspects | Autophagy (Cytology) | Neural circuitry | Observations | Huntingtons disease | Competition | Biotechnology | Huntingtin | Toxicity | Pathogenesis | Impairment | Biosynthesis | Kinases | Experiments | Degradation | Proteins | Scholarships & fellowships | Ataxin | Rodents | Spinocerebellar ataxia | Ataxia | Biocompatibility | Trinucleotide repeat diseases | Medical research | Starvation | Neurodegenerative diseases | Polyglutamine diseases | Huntington's disease | Neurological diseases | Machado-Joseph disease | Cell lines | Scientific imaging | Mass spectrometry | Phagocytosis | Index Medicus
Journal Article
Neurology, ISSN 0028-3878, 05/2007, Volume 68, Issue 19, pp. 1557 - 1562
Journal Article
The Lancet Neurology, ISSN 1474-4422, 2017, Volume 16, Issue 9, pp. 701 - 711
Journal Article