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通过将羊膜植入尾状核来逆转非人类灵长类动物的偏侧帕金森综合征。

Reversal of hemiparkinsonian syndrome in nonhuman primates by amnion implantation into caudate nucleus.

作者信息

Bankiewicz K S, Palmatier M, Plunkett R J, Cummins A, Oldfield E H

机构信息

Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland.

出版信息

J Neurosurg. 1994 Dec;81(6):869-76. doi: 10.3171/jns.1994.81.6.0869.

DOI:10.3171/jns.1994.81.6.0869
PMID:7965117
Abstract

Although recent animal and human experiments suggest that tissue implantation can ameliorate parkinsonism, there is controversy about what mechanism underlies recovery. Secretion of dopamine from the graft seems unlikely to be the sole restorative factor. Regenerative sprouting by the host brain may also underlie behavioral recovery. Fetal amnion and term amnion, which were shown to produce and secrete a factor that supports the outgrowth of neurite processes in vitro, were implanted in hemiparkinsonian monkeys. Fetal amnion implants induced sprouting of dopaminergic fibers from the host brain and behavioral improvement, despite failure of the grafts to survive. Animals implanted with term amnion also had some sprouted dopaminergic fibers and behavioral improvement, but these were limited and were similar to the recovery, in prior experiments using the same primate model of parkinsonism, of animals that received surgical cavitation only. Recovery after central nervous system grafting with fetal amnion, a fetal accessory tissue, does not require secretion of a deficient neurotransmitter(s) from the graft and occurs despite the failure of graft survival. Recovery after cerebral implantation of fetal tissues appears to depend more on the regenerative and recuperative processes of the host brain than on graft replacement of deficient neurotransmitters or development of functional synaptic connections between the graft and the host brain.

摘要

尽管最近的动物和人体实验表明组织植入可以改善帕金森症,但对于恢复的潜在机制仍存在争议。移植组织中多巴胺的分泌似乎不太可能是唯一的恢复因素。宿主大脑的再生性发芽也可能是行为恢复的基础。已证明能产生并分泌一种在体外支持神经突生长的因子的胎儿羊膜和足月羊膜,被植入患偏侧帕金森症的猴子体内。尽管移植组织未能存活,但胎儿羊膜植入仍诱导了宿主大脑多巴胺能纤维的发芽和行为改善。植入足月羊膜的动物也有一些发芽的多巴胺能纤维和行为改善,但这些都是有限的,并且类似于在先前使用相同帕金森症灵长类动物模型的实验中仅接受手术空洞化的动物的恢复情况。用胎儿羊膜(一种胎儿附属组织)进行中枢神经系统移植后的恢复并不需要移植组织分泌缺乏的神经递质,并且即使移植组织未能存活也会发生。胎儿组织脑内植入后的恢复似乎更多地取决于宿主大脑的再生和恢复过程,而不是移植组织对缺乏神经递质的替代或移植组织与宿主大脑之间功能性突触连接的形成。

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