REVERSAL OF HEMIPARKINSONIAN SYNDROME IN NONHUMAN-PRIMATES BY AMNION IMPLANTATION INTO CAUDATE-NUCLEUS

Although recent animal and human experiments suggest that tissue impla ntation can ameliorate parkinsonism, there is controversy about what m echanism underlies recovery. Secretion of dopamine from the graft seem s unlikely to be the sole restorative factor. Regenerative sprouting b y the host brain may also underlie behavioral recovery. Fetal amnion a nd term amnion, which were shown to produce and secrete a factor that supports the outgrowth of neurite processes in vitro, were implanted i n hemiparkinsonian monkeys. Fetal amnion implants induced sprouting of dopaminergic fibers from the host brain and behavioral improvement, d espite failure of the grafts to survive. Animals implanted with term a mnion also had some sprouted dopaminergic fibers and behavioral improv ement, but these were limited and were similar to the recovery, in pri or experiments using the same primate model of parkinsonism, of animal s that received surgical cavitation only. Recovery after central nervo us system grafting with fetal amnion, a fetal accessory tissue, does n ot require secretion of a deficient neurotransmitter(s) from the graft and occurs despite the failure of graft survival. Recovery after cere bral implantation of fetal tissues appears to depend more on the regen erative and recuperative processes of the host brain than on graft rep lacement of deficient neurotransmitters or development of functional s ynaptic connections between the graft and the host brain.