Abstract
Huntington’ disease (HD) is a neurodegenerative disease presently lacking effective therapy, even palliative. Striatal excitotoxic lesions in rats have served as useful models for HD but do not mimic the movement abnormalities of dyskinesia and chorea seen in HD. A nonhuman primate-model of HD by excitotoxic caudate and putamen lesions is developed to determine the underlying mechanisms for dyskinesias following basal ganglia lesions. This model is used to determine the effects of new therapeutic approaches such as neuronal transplantation. The model will also generate important information about the symptomatology of the disease as well as the likely pathological events in HD. As it is not known how long it will take to find the specific gene responsible for HD nor does how the effects of this gene can be modified to treat the disease, the excitotoxic lesion (EXL) model in the primate serve as a useful experimental analogy of HD. From this primate model, the symptoms pertaining to striatal dysfunction can be elucidated and, above all, the therapeutic strategies for HD that may merge with clinical studies and practice can be tested.
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