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Fetal striatal allografts reverse cognitive deficits in a primate model of Huntington disease

Abstract

Substitutive therapy using fetal striatal grafts in animal models of Huntington disease (HD) have already demonstrated obvious beneficial effects on motor indices1. Using a new phenotypic model of HD recently designed in primates2,3, we demonstrate here complete and persistent recovery in a frontal-type cognitive task two to five months after intrastriatal allografting. The striatal allografts also reduce the occurence of dystonia, a major abnormal movement associated with HD. These results show the capacity of fetal neurons to provide a renewed substrate for both cognitive and motor systems in the lesioned adult brain. They also support the use of neural transplantation as a potential therapy for HD.

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Palfi, S., Condé, F., Riche, D. et al. Fetal striatal allografts reverse cognitive deficits in a primate model of Huntington disease. Nat Med 4, 963–966 (1998). https://doi.org/10.1038/nm0898-963

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