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1. Full Text One decade ago, one decade ahead in huntington's disease
by Wild, Edward J and Tabrizi, Sarah J
Movement Disorders, ISSN 0885-3185, 10/2019, Volume 34, Issue 10, pp. 1434 - 1439
neurodegeneration | antisense therapy | Huntington's disease | huntingtin | Medicine, Experimental | Medical research
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2. Full Text Huntingtin Lowering Strategies for Disease Modification in Huntington's Disease
by Tabrizi, Sarah J and Ghosh, Rhia and Leavitt, Blair R
Neuron, ISSN 0896-6273, 03/2019, Volume 101, Issue 5, pp. 801 - 819
In this review, Tabrizi et al. describe new approaches to disease modification in Huntington's disease. These aim to reduce mutant huntingtin protein by... 
genome editing | proteolysis-targeting chimeras | HD biomarkers | RNAi | CRISPR/Cas9 | antisense oligonucleotides | drug delivery | Huntington's disease | transcription activator-like effector nucleases | zinc-finger proteins | small-molecule splicing modulators | CAG REPEAT | POTENTIAL THERAPY | YAC128 MOUSE MODEL | NEUROFILAMENT LIGHT PROTEIN | MUTANT HUNTINGTIN | EMBRYONIC LETHALITY | CEREBROSPINAL-FLUID | ANTISENSE OLIGONUCLEOTIDES | NEUROSCIENCES | MOTOR DYSFUNCTION | MOLECULAR-MECHANISMS | Drugs | Medical research | Nucleases | Nervous system diseases | Drug delivery systems | Genomics | DNA binding proteins | Genetic transcription | Vehicles | Proteolysis | Medical genetics | Medicine, Experimental | Research institutes
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3. Full Text Huntingtin Lowering Strategies for Disease Modification in Huntington’s Disease
by Tabrizi, Sarah J and Ghosh, Rhia and Leavitt, Blair R
Neuron, ISSN 0896-6273, 03/2019, Volume 101, Issue 5, pp. 801 - 819
Huntington’s disease is caused by an abnormally expanded CAG repeat expansion in the gene, which confers a predominant toxic gain of function in the mutant... 
genome editing | proteolysis-targeting chimeras | RNAi | HD biomarkers | CRISPR/Cas9 | antisense oligonucleotides | Huntington’s disease | drug delivery | zinc-finger proteins | transcription activator-like effector nucleases | small-molecule splicing modulators | Huntingtons disease | Post-transcription | Huntingtin | Neuropathology | Pathogenesis | Genes | Clinical trials | Proteins | Genotype & phenotype | Proteolysis | Fibroblasts | Zinc finger proteins | Chimeras | Trinucleotide repeat diseases | Deoxyribonucleic acid--DNA | University colleges | CRISPR | Polyglutamine | Splicing | RNA-mediated interference | Trinucleotide repeats | Antisense RNA | Antisense oligonucleotides | Pathology | Brain research | Mutation | Pharmaceuticals
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4. Full Text Huntingtin Lowering Strategies for Disease Modification in Huntington’s Disease
by Tabrizi, Sarah J and Ghosh, Rhia and Leavitt, Blair R
Neuron, ISSN 0896-6273, 05/2019, Volume 102, Issue 4, pp. 899 - 899
Huntingtons disease | Huntingtin
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5. Clinical features of huntington’s disease
by Ghosh, Rhia and Tabrizi, Sarah J
Advances in Experimental Medicine and Biology, ISSN 0065-2598, 2018, Volume 1049, pp. 1 - 28
Therapeutics | Biomarkers | Genetics | Huntington’s disease | Management | Symptoms
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6. Clinical Features of Huntington's Disease
by Ghosh, Rhia and Tabrizi, Sarah J
Advances in experimental medicine and biology, ISSN 0065-2598, 2018, Volume 1049, p. 1
Huntington's disease (HD) is the most common monogenic neurodegenerative disease and the commonest genetic dementia in the developed world. With autosomal... 
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7. Full Text Huntingtin Lowering Strategies for Disease Modification in Huntington's Disease (vol 101, pg 801, 2019)
by Tabrizi, SJ and Ghosh, R and Leavitt, BR
NEURON, ISSN 0896-6273, 05/2019, Volume 102, Issue 4, pp. 899 - 899
NEUROSCIENCES
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8. Full Text Stimulating neural plasticity with real‐time fMRI neurofeedback in Huntington's disease: A proof of concept study
by Papoutsi, Marina and Weiskopf, Nikolaus and Langbehn, Douglas and Reilmann, Ralf and Rees, Geraint and Tabrizi, Sarah J
Human Brain Mapping, ISSN 1065-9471, 03/2018, Volume 39, Issue 3, pp. 1339 - 1353
Novel methods that stimulate neuroplasticity are increasingly being studied to treat neurological and psychiatric conditions. We sought to determine whether... 
neurodegenerative diseases | real‐time fMRI | neurofeedback training | Huntington's disease | brain training | neuroplasticity | real-time fMRI | TRACK-HD | RESONANCE-IMAGING NEUROFEEDBACK | HUMAN BRAIN | SELF-REGULATION | PREMANIFEST | NEUROSCIENCES | NEUROIMAGING | CONNECTIVITY | CLINICAL-TRIALS | COGNITIVE ASSESSMENT | RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING | MICROSTRUCTURE | PROGRESSION | Motor Activity - physiology | Humans | Huntington Disease - pathology | Middle Aged | Magnetic Resonance Imaging - methods | Male | Volition - physiology | Neuronal Plasticity - physiology | Cognition - physiology | Adult | Female | Neurofeedback - methods | Huntington Disease - physiopathology | Putaminal Hemorrhage - physiopathology | Organ Size | Motor Cortex - physiopathology | Motor Cortex - pathology | Proof of Concept Study | Gray Matter - diagnostic imaging | Huntington Disease - diagnostic imaging | Motor Cortex - diagnostic imaging | Learning - physiology | Gray Matter - pathology | Putaminal Hemorrhage - diagnostic imaging | Brain Mapping | Aged | Neurofeedback - physiology | Medicine, Experimental | Medical research | Biofeedback training | Nervous system diseases | Magnetic resonance imaging | Huntingtons disease | Neuroimaging | Brain | Cognitive ability | Motor task performance | Substantia grisea | Plasticity (neural) | Plasticity (functional) | Training | Plasticity (behavioral) | Functional anatomy | Feedback | Neurodegeneration | Functional magnetic resonance imaging | Supplementary motor area | Medical imaging | Cortex | Brain mapping | Feasibility studies | Real time | Patients | Putamen | Neurology | Neural networks | Structure-function relationships
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9. Full Text E01 Modelling the trajectory of cortical atrophy in huntington’s disease
by Eileanoir B Johnson and Gabriel Ziegler and Will Penny and Geraint Rees and Sarah J Tabrizi and Rachael I Scahill and Sarah Gregory
Journal of Neurology, Neurosurgery and Psychiatry, ISSN 0022-3050, 09/2018, Volume 89, Issue Suppl 1, p. A35
Background Despite histological evidence of widespread grey matter atrophy by end-stage Huntington’s disease (HD), the progression of cortical atrophy in HD... 
Atrophy
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10. Full Text Therapies targeting DNA and RNA in Huntington's disease
by Wild, Edward J and Tabrizi, Sarah J
The Lancet Neurology, ISSN 1474-4422, 10/2017, Volume 16, Issue 10, pp. 837 - 847
No disease-slowing treatment exists for Huntington's disease, but its monogenic inheritance makes it an appealing candidate for the development of therapies... 
CAG REPEAT | TRACK-HD | SPINAL MUSCULAR-ATROPHY | POTENTIAL THERAPY | OBSERVATIONAL DATA | MOUSE MODEL | CLINICAL-TRIALS | GENE-THERAPY | CEREBROSPINAL-FLUID | ANTISENSE OLIGONUCLEOTIDES | CLINICAL NEUROLOGY | Huntington Disease - therapy | Huntingtin Protein | Animals | Biological Therapy - methods | RNA | DNA | Humans | Genetic research | Genetic translation | Huntingtons disease | Brain | Animal models | Transcription factors | Transcription | Huntingtin | Clinical trials | Genomes | Proteins | Repressors | Neurodegeneration | Zinc finger proteins | Trinucleotide repeat diseases | CRISPR | Polyglutamine | RNA-mediated interference | Trinucleotide repeats | Cell division | Antisense RNA | Federal regulation | Antisense oligonucleotides | Heredity | FDA approval | Huntington's disease | Gene expression | Genetic engineering | Antisense DNA | Mutation | Gene therapy
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11. Full Text The pathogenic exon 1 HTT protein is produced by incomplete splicing in Huntington's disease patients
by Neueder, Andreas and Landles, Christian and Ghosh, Rhia and Howland, David and Myers, Richard H and Faull, Richard L. M and Tabrizi, Sarah J and Bates, Gillian P
Scientific Reports, ISSN 2045-2322, 12/2017, Volume 7, Issue 1, p. 1307
We have previously shown that exon 1 of the huntingtin gene does not always splice to exon 2 resulting in the production of a small polyadenylated mRNA... 
CAG REPEAT | R6/2 | INSTABILITY | MULTIDISCIPLINARY SCIENCES | MUTANT HUNTINGTIN | LENGTH | GENE-EXPRESSION | IN MOUSE MODEL | ANTISENSE OLIGONUCLEOTIDES | BRAIN | TRANSGENIC MICE
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12. Full Text In vivo neutralization of the protagonist role of macrophages during the chronic inflammatory stage of Huntington’s disease
by Pido-Lopez, Jeffrey and Andre, Ralph and Benjamin, Agnesska C and Ali, Nadira and Farag, Sahar and Tabrizi, Sarah J and Bates, Gillian P
Scientific Reports, ISSN 2045-2322, 12/2018, Volume 8, Issue 1, pp. 1 - 14
Neurodegenerative diseases, characterised by the progressive and selective neuronal death in the central nervous system, are frequently accompanied by an... 
Huntingtons disease | Phenotypes | Animal models | Immune response | Neurodegenerative diseases | Immunomodulation | Central nervous system | Inflammation | Macrophages | Huntington's disease | Bisphosphonates | Immunosuppressive agents | Clodronic acid | Monocytes | Immune system
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13. Full Text Huntington's disease: from molecular pathogenesis to clinical treatment
by Ross, Christopher A, Dr and Tabrizi, Sarah J, FRCP
Lancet Neurology, The, ISSN 1474-4422, 2011, Volume 10, Issue 1, pp. 83 - 98
Summary Huntington's disease is a progressive, fatal, neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin gene, which encodes an... 
Neurology | UBIQUITIN-PROTEASOME SYSTEM | IN-VIVO | MUTANT-HUNTINGTIN | MITOCHONDRIAL DYSFUNCTION | R6/2 MOUSE MODEL | HISTONE DEACETYLASE INHIBITORS | POLYGLUTAMINE AGGREGATION | INCLUSION-BODY FORMATION | NEURODEGENERATIVE DISEASES | CLINICAL NEUROLOGY | AGE-OF-ONSET | Nerve Tissue Proteins - history | Neurons - pathology | History, 20th Century | Humans | Huntington Disease - pathology | Peptides - genetics | Magnetic Resonance Imaging - methods | Nuclear Proteins - chemistry | Nerve Tissue Proteins - genetics | Disease Progression | Huntington Disease - therapy | Huntingtin Protein | Nerve Tissue Proteins - chemistry | Animals | Nuclear Proteins - history | Models, Biological | Brain - pathology | Huntington Disease - genetics | Neurons - metabolism | Nuclear Proteins - genetics | Disease Models, Animal | Proteins | Development and progression | Nervous system diseases | Diagnostic imaging | Parkinson's disease | Huntington's chorea | Index Medicus
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14. Full Text Inhibition of tumour necrosis factor alpha in the R6/2 mouse model of Huntington’s disease by etanercept treatment
by Pido-Lopez, Jeffrey and Tanudjojo, Benedict and Farag, Sahar and Bondulich, Marie-Katrin and Andre, Ralph and Tabrizi, Sarah J and Bates, Gillian P
Scientific Reports, ISSN 2045-2322, 12/2019, Volume 9, Issue 1, pp. 1 - 12
Huntington’s disease (HD) is an inherited neurodegenerative disorder caused by the expansion of the CAG repeat in exon 1 of the huntingtin (HTT) gene, which... 
Huntingtons disease | Animal models | Polyglutamine | Immune response | Huntingtin | Cytokines | Neurodegenerative diseases | Trinucleotide repeats | Inflammation | Tumor necrosis factor-α | Huntington's disease | Interleukin 6 | Neurotoxicity | Etanercept | Rodents | Neostriatum | Plasma levels | Trinucleotide repeat diseases | Tumors
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15. Full Text A30 The role of huntingtin in human myeloid cells
by Ralph Andre and Grace O’Regan and Sahar Farag and Paul Lavender and Sarah J Tabrizi
Journal of Neurology, Neurosurgery and Psychiatry, ISSN 0022-3050, 09/2018, Volume 89, Issue Suppl 1, p. A11
Background While the central nervous system is considered to be the primary site of Huntington’s disease pathology, the systemic innate immune system may be a... 
Genotype & phenotype | Cytokines | Immune system
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16. Full Text F22 Robust biomarkers of huntington’s disease progression: observations from the track-hd, predict-hd and image-hd studies
by Peter A Wijeratne and Eileanoir B Johnson and Sarah Gregory and Amrita Mohan and Cristina Sampaio and Rachael I Scahill and Sarah J Tabrizi and Daniel C Alexander
Journal of Neurology, Neurosurgery and Psychiatry, ISSN 0022-3050, 09/2018, Volume 89, Issue Suppl 1, p. A47
Background The TRACK, PREDICT and IMAGE-HD studies provide rich and varied datasets with which to identify robust imaging and clinical biomarkers of... 
Biomarkers
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