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Journal Article
1993, ISBN 0521459834, Volume 23., 46
This report presents the findings of a study of people affected by Huntington's chorea and their unaffected relatives, and in particular, of the incidence of... 
Book
2002, 3rd ed., Oxford monographs on medical genetics, ISBN 0198510608, Volume 45, xvi, 558
Book
1989, Johns Hopkins series in contemporary medicine and public health., ISBN 0801838606, x, 251
Book
1981, ISBN 0387105883, xvii, 192
Book
PloS one, ISSN 1932-6203, 2012, Volume 7, Issue 12, p. e50717
Huntington's disease (HD) is an autosomal neurodegenerative disorder, characterized by severe behavioral, cognitive, and motor deficits. Since the discovery of... 
CAG REPEAT | STRIATAL NEURONAL LOSS | BASAL GANGLIA | H-1 MRS | MULTIDISCIPLINARY SCIENCES | HD GENE | SPINY NEURONS | BLOOD-FLOW | CORTICOSTRIATAL PATHWAY | EARLY MOTOR | TRINUCLEOTIDE REPEAT | Neurons - pathology | Body Weight | Cell Count | Huntington Disease - pathology | Male | Synaptic Transmission | Behavior, Animal | Brain - metabolism | Endpoint Determination | Female | Glutamic Acid - secretion | Swimming | Huntington Disease - physiopathology | Disease Models, Animal | Neostriatum - pathology | Magnetic Resonance Spectroscopy | Brain - physiopathology | Organ Size | Huntington Disease - metabolism | Nerve Tissue Proteins - genetics | Disease Progression | Gene Knock-In Techniques | Neurophysiology | Magnetic Resonance Imaging | Animals | Brain - pathology | Huntington Disease - genetics | Repetitive Sequences, Nucleic Acid | Mice | Taurine | Brain | Nervous system diseases | Magnetic resonance imaging | Genetic aspects | Glutamine | Huntingtons disease | Nuclear magnetic resonance--NMR | Huntingtin | Brain slice preparation | Cognitive ability | Heterozygotes | Creatine | Experiments | Magnetic resonance spectroscopy | Rodents | Spectrum analysis | Neostriatum | Physiology | Age | Spectroscopy | Neurodegenerative diseases | Neurons | Cortex | Phosphocreatine | Metabolism | Huntington's disease | Spiny neurons | Homozygotes | Neurology | Brain research | Reproducibility | Biomarkers | Glutamatergic transmission | Mutation | Laboratory animals | N-Acetylaspartate | Animal cognition | Nuclear magnetic resonance | NMR
Journal Article
PloS one, ISSN 1932-6203, 2014, Volume 9, Issue 9, p. e107434
Huntington disease (HD) is an inherited, fatal neurodegenerative disorder caused by a CAG repeat expansion in the huntingtin gene. The mutant protein causes... 
SELECTIVE INHIBITION | CAG REPEATS | RNA DUPLEXES | NUCLEIC-ACID | MULTIDISCIPLINARY SCIENCES | MOUSE MODEL | ATAXIN-3 | EMBRYONIC LETHALITY | EXPRESSION | SINGLE-NUCLEOTIDE POLYMORPHISMS | MOLECULAR-MECHANISMS | Genetic Therapy | Neurons - pathology | Embryo, Mammalian | Humans | Huntington Disease - pathology | Molecular Sequence Data | Structure-Activity Relationship | Huntington Disease - therapy | RNA Interference | Base Sequence | Drug Design | Female | Neurons - metabolism | Nerve Tissue Proteins - antagonists & inhibitors | Gene Expression | Oligonucleotides, Antisense - chemistry | Hippocampus - pathology | Huntington Disease - metabolism | Nerve Tissue Proteins - genetics | Nerve Tissue Proteins - metabolism | Hippocampus - metabolism | Huntingtin Protein | Animals | Oligonucleotides, Antisense - genetics | Alleles | Huntington Disease - genetics | Mice | Polymorphism, Single Nucleotide | Mutation | Primary Cell Culture | Nervous system diseases | Single nucleotide polymorphisms | Huntington's chorea | Health aspects | Neurophysiology | Huntingtons disease | Disease | Huntingtin | Pathogenesis | Cognitive ability | Oligonucleotides | Single-nucleotide polymorphism | Drug delivery | Proteins | Wings | Neurodegeneration | Rodents | Degeneration | Trinucleotide repeat diseases | Polyglutamine | Neurodegenerative diseases | Medical treatment | Trinucleotide repeats | Antisense oligonucleotides | Huntington's disease | Gene expression | Disease control | Medicine | Acids | Apoptosis | Pharmaceuticals
Journal Article
Neuroscience, ISSN 0306-4522, 2019, Volume 403, pp. 79 - 92
Highlights • The macromolecular proton fraction (MMPF), an MRI marker of myelin, was reduced in Huntington’s disease (HD). • MMPF reductions in white matter... 
Neurology | myelin | white matter | Huntington’s disease | basal ganglia | cognition | clinical markers | Huntington's disease | HUMAN BRAIN | ABNORMALITIES | TRACTS | PATHOLOGY | NEUROSCIENCES | EXPLORATORY FACTOR-ANALYSIS | TENSOR | CONNECTIVITY | INTEGRITY | COGNITIVE ASSESSMENT | WHITE-MATTER MICROSTRUCTURE | Brain - diagnostic imaging | White Matter - metabolism | Humans | Huntington Disease - pathology | Middle Aged | Huntington Disease - psychology | Magnetic Resonance Imaging - methods | Male | Cognition | Neural Pathways - pathology | Myelin Sheath - metabolism | Young Adult | Multimodal Imaging | Adult | Female | Imaging, Three-Dimensional | Executive Function | Organ Size | Huntington Disease - metabolism | White Matter - pathology | Huntington Disease - diagnostic imaging | White Matter - diagnostic imaging | Neural Pathways - diagnostic imaging | Brain - pathology | Neural Pathways - metabolism | Memory, Short-Term | Medical research | Nervous system diseases | Neurosciences | Magnetization | Huntington's chorea | Anisotropy | Radiation | Medicine, Experimental | FA, fractional anisotropy | CC, corpus callosum | CST, cortico-spinal tract | FWE, Free Water Elimination | PCA, principal component analysis | RD, radial diffusivity | qMT, quantitative magnetization transfer | SMA, supplementary motor area | MoCA, Montreal Cognitive Assessment | DSST, Digit Symbol Substitution Test | ATR, anterior thalamic radiation | YoE, years of education | HARDI, high angular resolution diffusion imaging | fODFs, fiber orientation density functions | SPGR, spoiled gradient recalled-echo | BG, basal ganglia | ROI, region of interest | WM, white matter | AD, axial diffusivity | MMPF, macromolecular proton fraction | PFC, prefrontal cortex | dRL, damped Richardson-Lucy algorithm | HD, Huntington’s disease
Journal Article
PloS one, ISSN 1932-6203, 2016, Volume 11, Issue 2, p. e0148839
Huntington's disease (HD) is caused by an expansion of the trinucleotide poly (CAG) tract located in exon 1 of the huntingtin (Htt) gene leading to progressive... 
NUCLEAR-LOCALIZATION | MAGNETIC-RESONANCE-SPECTROSCOPY | MESSENGER-RNA | PROTEIN LENGTH | LEVELS DECREASE | MULTIDISCIPLINARY SCIENCES | MUTANT HUNTINGTIN | GENE-EXPRESSION | ENERGY-METABOLISM | STRIATAL NEURONS | TRANSGENIC MICE | Neuroimaging | Motor Skills - physiology | Huntington Disease - pathology | Huntington Disease - psychology | Mice, Transgenic - genetics | Male | Mice, Transgenic - metabolism | Huntington Disease - metabolism | Blotting, Western | Gene Knock-In Techniques | Atrophy | Brain - metabolism | Magnetic Resonance Imaging | Serotonin Plasma Membrane Transport Proteins - genetics | Animals | Brain - pathology | Huntington Disease - genetics | Female | Mice | Huntington Disease - physiopathology | Disease Models, Animal | Huntington's chorea | Physiological aspects | Development and progression | Genetic aspects | Models | Research | Gene expression | Huntingtons disease | Brain | Neurosciences | Animal models | Huntingtin | Neuropathology | Neurobiology | Cognitive ability | Males | Proteins | Metabolites | Transgenic animals | Neurodegeneration | Rodents | Neostriatum | Genetics | Age | Dopamine | Polyglutamine | Committees | Trinucleotide repeats | Behavioral sciences | Metabolism | Huntington's disease | Medicine | Neurology | Magnetic resonance imaging | Point mutation | Mutation | Laboratory animals | Psychiatry | Animal cognition
Journal Article
by Langbehn, Douglas and Leavitt, Blair R and Roos, Raymund and Durr, Alexandra and Mead, Simon and Holmans, Peter and Jones, Lesley and Tabrizi, Sarah J and Santos, R Dar and Decolongon, J and Sturrock, A and Ret, C Jauff and Lehericy, S and Marelli, C and Nigaud, K and Valabrègue, R and van den Bogaard, SJA and van der Grond, J and Arran, N and Callaghan, J and Hobbs, N and Lahiri, N and Ordidge, R and Owen, G and Read, J and Say, M and Patel, A and Fox, N C and Gibbard, C and Whitehead, D and Keenan, S and Berna, C and Bohlen, S and Man, A Hoff and Acharya, T and Lee, S and Monaco, W and Campbell, C and Queller, S and Whitlock, K and Campbell, M and Frajman, E and Milchman, C and O'Regan, A and Labuschagne, I and Stout, J and Scahill, R and Hicks, S and Tobin, A and Rosas, HD and Reilmann, R and Borowsky, B and Pourchot, C and Bachoud-Lévi, Anne-Catherine and Bentivoglio, Anna Rita and Biunno, Ida and Bonelli, Raphael and Burgunder, Jean-Marc and Dunnett, Stephen and Ferreira, Joaquim and Heiberg, Arvid and Illmann, Torsten and Landwehrmeyer, G. Bernhard and Levey, Jamie and Ramos-Arroyo, Maria A and Koivisto, Susana Pro and Roos, Raymund A.C and Sebastián, A Rojo and Tabrizi, Sarah and Vandenberghe, Wim and Uhrova, Tereza and Wahlström, Jan and Zaremba, Jacek and Baake, Verena and Barth, Katrin and Garde, Monica Bascuñana and Bos, Reineke and Callaghan, Jenny and Guedes, Leonor Correia and Finisterra, Ana Maria and Gilling, Mette and Hvalstedt, Carina and Held, Christine and Koppers, Kerstin and Laurà, Matilde and Descals, Asunción Martínez and Martinez-Horta, Saül and Mestre, Tiago and Monza, Daniela and Mütze, Lisanne and Oehmen, Martin and Orth, Michael and Padieu, Hélène and Paterski, Laurent and Peppa, Nadia and Rialland, Amandine and Šašinková, Pavla and Timewell, Erika and Cubillo, Patricia Trigo and da Silva, Wildson Vieira and ... and TRACK-HD investigators and REGISTRY investigators and TRACK-HD Investigators and REGISTRY Investigators
Lancet neurology, ISSN 1474-4422, 2017, Volume 16, Issue 9, pp. 701 - 711
Journal Article