Expanding the genetics of huntingtonism

Neurology

Volumn 82, Issue 4, 2014, Pages 286-287

  Feigin, Andrew ^a   Talbot, Kevin ^b  

^a FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH   (United States)

^b UNIVERSITY OF OXFORD   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

HIGH DENSITY LIPOPROTEIN 2;

AMYOTROPHIC LATERAL SCLEROSIS; CEREBELLAR ATAXIA; CLINICAL FEATURE; COGNITIVE DEFECT; EDITORIAL; EYE MOVEMENT DISORDER; FAMILY HISTORY; GENE MUTATION; GENETIC COUNSELING; GENETIC SCREENING; HUMAN; HUNTINGTON CHOREA; HUNTINGTON DISEASE LIKE SYNDROME; HYPERREFLEXIA; MOTOR DYSFUNCTION; NEUROACANTHOCYTOSIS; PARANEOPLASTIC SYNDROME; PARKINSON DISEASE; PARKINSONISM; PRIORITY JOURNAL; TERTIARY CARE CENTER;

HUMANS; HUNTINGTON DISEASE; MUTATION; PROTEINS;

EID: 84895741569     PISSN: 00283878     EISSN: 1526632X     Source Type: Journal    
DOI: 10.1212/WNL.0000000000000067     Document Type: Editorial

References (4)

1. Walker FO. Huntington's disease. Lancet 2007;369:218-228.
2. Schneider SA, Walker RH, Bhatia KP. The Huntington's disease-like syndromes: What to consider in patients with a negative Huntington's disease gene test. Nat Clin Pract Neurol 2007;3:517-525.
3. Hensman Moss DJ, Poulter M, Beck J, et al. C9orf72 expansions are the most common genetic cause of Huntington disease phenocopies. Neurology 2014;82:292-299.
4. Mahoney CJ, Beck J, Rohrer JD, et al. Frontotemporal dementia with the C9ORF72 hexanucleotide repeat expansion: Clinical, neuroanatomical and neuropathological features. Brain 2012;135:736-750.