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

被引：117

作者：

Palfi, S

Condé, F

Riche, D

Brouillet, E

Dautry, C

Mittoux, V

Chibois, A

Peschanski, M

Hantraye, P

机构：

[1] Serv Hosp Frederic Joliot, CNRS,URA 2210, CEA, DSV,DRM, F-91401 Orsay, France

[2] Fac Med, INSERM, U421, F-94010 Creteil, France

来源：

NATURE MEDICINE | 1998年 / 4卷 / 08期

关键词：

D O I：

10.1038/nm0898-963

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Substitutive therapy using fetal striatal grafts in animal models of Huntington disease (HD) have already demonstrated obvious beneficial effects on motor indices(1). Using a new phenotypic model of HD recently designed in primates(2,3), 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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收藏

页码：963 / 966

页数：4

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