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Article
Nature Medicine  4, 963 - 966 (1998)
doi:10.1038/nm0898-963

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

Stéphane Palfi1, Françoise Condé1, Danielle Riche2, Emmanuel Brouillet1, Caroline Dautry1, Vincent Mittoux1, Anne Chibois1, Marc Peschanski2 & Philippe Hantraye1, 3

  1CEA CNRS URA 2210, Service Hospitaller Frédéric Joliot, CEA, DSV, DRM, 4 place du Général Leclerc, 91401 Orsay cedex, France

  2INSERM U-421, IM3, Faculté de Médecine, 8 rue du Général Sarrail, 94010 Créteil cedex, France

  3Correspondence should be addressed to P.H.; e-mail: hantraye@uriens.shfl.cea.fr

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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