Author
Listed:
- Shang-Hsun Yang
(Yerkes National Primate Research Center,
Department of Human Genetics,
Genetics and Molecular Biology Program,)
- Pei-Hsun Cheng
(Yerkes National Primate Research Center,
Department of Human Genetics,)
- Heather Banta
(Yerkes National Primate Research Center,)
- Karolina Piotrowska-Nitsche
(Yerkes National Primate Research Center,
Department of Human Genetics,
Institute of Genetics and Animal Breeding, Polish Academy of Sciences)
- Jin-Jing Yang
(Yerkes National Primate Research Center,
Department of Human Genetics,)
- Eric C. H. Cheng
(Yerkes National Primate Research Center,
Department of Human Genetics,)
- Brooke Snyder
(Yerkes National Primate Research Center,
Department of Human Genetics,)
- Katherine Larkin
(Yerkes National Primate Research Center,)
- Jun Liu
(Yerkes National Primate Research Center,
Department of Human Genetics,
Neuroscience Program,)
- Jack Orkin
(Yerkes National Primate Research Center,)
- Zhi-Hui Fang
(Department of Human Genetics,)
- Yoland Smith
(Yerkes National Primate Research Center,
Neuroscience Program,
Department of Neurology,)
- Jocelyne Bachevalier
(Yerkes National Primate Research Center,
Department of Psychology,
Emory University, Atlanta, Georgia 30329, USA)
- Stuart M. Zola
(Yerkes National Primate Research Center,
Neuroscience Program,
Emory University, Atlanta, Georgia 30329, USA
Veterans Affairs Medical Center, Atlanta, Georgia 30033, USA)
- Shi-Hua Li
(Department of Human Genetics,)
- Xiao-Jiang Li
(Department of Human Genetics,
Genetics and Molecular Biology Program,
Neuroscience Program,)
- Anthony W. S. Chan
(Yerkes National Primate Research Center,
Department of Human Genetics,
Genetics and Molecular Biology Program,
Neuroscience Program,)
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.
Suggested Citation
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 Smit, 2008.
"Towards a transgenic model of Huntington’s disease in a non-human primate,"
Nature, Nature, vol. 453(7197), pages 921-924, June.
Handle:
RePEc:nat:nature:v:453:y:2008:i:7197:d:10.1038_nature06975
DOI: 10.1038/nature06975
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