Towards a transgenic model of Huntington’s disease in a non-human primate

Shang-Hsun Yang, Pei-Hsun Cheng, Heather Banta, Karolina Piotrowska-Nitsche, Jin-Jing Yang, Eric C. H. Cheng, Brooke Snyder, Katherine Larkin, Jun Liu, Jack Orkin, Zhi-Hui Fang, Yoland Smith, Jocelyne Bachevalier, Stuart M. Zola, Shi-Hua Li, Xiao-Jiang Li and Anthony W. S. Chan ()
Additional contact information
Shang-Hsun Yang: Yerkes National Primate Research Center,
Pei-Hsun Cheng: Yerkes National Primate Research Center,
Heather Banta: Yerkes National Primate Research Center,
Karolina Piotrowska-Nitsche: Yerkes National Primate Research Center,
Jin-Jing Yang: Yerkes National Primate Research Center,
Eric C. H. Cheng: Yerkes National Primate Research Center,
Brooke Snyder: Yerkes National Primate Research Center,
Katherine Larkin: Yerkes National Primate Research Center,
Jun Liu: Yerkes National Primate Research Center,
Jack Orkin: Yerkes National Primate Research Center,
Zhi-Hui Fang: Department of Human Genetics,
Yoland Smith: Yerkes National Primate Research Center,
Jocelyne Bachevalier: Yerkes National Primate Research Center,
Stuart M. Zola: Yerkes National Primate Research Center,
Shi-Hua Li: Department of Human Genetics,
Xiao-Jiang Li: Department of Human Genetics,
Anthony W. S. Chan: Yerkes National Primate Research Center,

Nature, 2008, vol. 453, issue 7197, 921-924

Abstract: Huntington's disease: Model answers Huntington's disease is a severely disabling and lethal neurodegenerative disorder. The development of a non-human primate model for the disease would be invaluable in understanding its pathology and in developing therapeutic strategies, and this paper reports a significant step towards that goal is reported in this issue. Transgenic rhesus macaque monkeys that express the first exon of the polyglutamine-expanded human huntingtin gene develop key features of Huntington's disease, including dystonia and chorea. The data suggest that it will be feasible to generate non-human primate models for Huntington's disease and possibly for other neurodegenerative disorders, where rodent models may not reflect the brain changes and behavioural features of the human disease.

Date: 2008
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DOI: 10.1038/nature06975

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