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

Palfi S, Conde F, Riche D, Brouillet E, Dautry C, Mittoux V, Chibois A, Peschanski M, Hantraye P
Nat Med 1998 Aug;4(8):963-6
Palfi-1998
CEA CNRS URA 2210, Service Hospitalier Frederic Joliot, CEA, DSV, DRM, Orsay, France. Substitutive therapy using fetal striatal grafts in animal model of Huntington disease (HD) have already demonstrated obvious beneficial effects on motor indices. Using a new phenotypic model of HD recently designed in primates, 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 occurrence 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.