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

Nat Med. 1998 Aug;4(8):963-6. doi: 10.1038/nm0898-963.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apomorphine / pharmacology
  • Brain Tissue Transplantation*
  • Cognition*
  • Corpus Striatum / physiology
  • Corpus Striatum / transplantation*
  • Fetal Tissue Transplantation*
  • Huntington Disease / chemically induced
  • Huntington Disease / psychology*
  • Huntington Disease / surgery*
  • Macaca fascicularis
  • Magnetic Resonance Imaging
  • Motor Activity / drug effects
  • Nitro Compounds
  • Propionates
  • Transplantation, Homologous


  • Nitro Compounds
  • Propionates
  • Apomorphine
  • 3-nitropropionic acid