Fetal striatal allografts reverse cognitive deficits in a primate model of Huntington disease.
Substitutive therapy using fetal striatal grafts in animal models 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.
Palfi
S
S
CEA CNRS URA 2210, Service Hospitalier Frédéric Joliot, CEA, DSV, DRM, Orsay, France.
Condé
F
F
Riche
D
D
Brouillet
E
E
Dautry
C
C
Mittoux
V
V
Chibois
A
A
Peschanski
M
M
Hantraye
P
P
D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D016380:Brain Tissue Transplantation; D003071:Cognition; D003342:Corpus Striatum / Q000502:physiology / Q000637:transplantation*; D016332:Fetal Tissue Transplantation; D006816:Huntington Disease / Q000139:chemically induced / Q000523:psychology* / Q000601:surgery*; D008252:Macaca fascicularis; D008279:Magnetic Resonance Imaging; D009043:Motor Activity / Q000187:drug effects; D009574:Nitro Compounds; D011422:Propionates; D014184:Transplantation, Homologous
D009574:Nitro Compounds; D011422:Propionates; D001058:Apomorphine; C015392:3-nitropropionic acid