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FUNCTIONAL RECOVERY IN PARKINSONIAN MONKEYS TREATED WITH GDNF

机译：GDNF处理的帕金森猴中的功能恢复

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摘要

PARKINSON's disease results from the progressive degeneration of dopamine neurons that innervate the striatum(1,2). In rodents, glial-cell-line-derived neurotrophic factor (GDNF) stimulates an increase in midbrain dopamine levels, protects dopamine neurons from some neurotoxins, and maintains injured dopamine neurons(3-9). Here we extend the rodent studies to an animal closer to the human in brain organization and function, by evaluating the effects of GDNF injected intracerebrally into rhesus monkeys that have had the symptomatology and pathophysiological features of Parkinson's disease induced by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)(10-14). The recipients of GDNF displayed significant improvements in three of the cardinal symptoms of parkinsonism: bradykinesia, rigidity and postural instability. GDNF administered every four weeks maintained functional recovery. On the lesioned side of GDNF-treated animals, dopamine levels in the midbrain and globus pallidus were twice as high, and nigral dopamine neurons were, on average, 20% larger, with an increased fibre density. The results indicate that GDNF may be of benefit in the treatment of Parkinson's disease. [References: 22]
机译：帕金森氏病是由支配纹状体的多巴胺神经元进行性变性引起的（1,2）。在啮齿动物中，胶质细胞系衍生的神经营养因子（GDNF）刺激中脑多巴胺水平升高，保护多巴胺神经元免受某些神经毒素的侵害，并维持受损的多巴胺神经元（3-9）。在这里，我们通过评估脑内注射到具有由神经毒素1-甲基-4诱发的帕金森氏病的症状和病理生理特征的恒河猴中的GDNF的作用，将啮齿动物研究扩展到大脑组织和功能更接近人类的动物-苯基-1,2,3,6-四氢吡啶（MPTP）（10-14）。 GDNF的接受者对帕金森氏症的三个主要症状表现出明显改善：运动迟缓，僵硬和姿势不稳。每四周施用的GDNF维持功能恢复。在受GDNF处理的动物的患侧，中脑和苍白球的多巴胺水平高一倍，而黑质多巴胺神经元平均大20％，且纤维密度增加。结果表明GDNF可能在帕金森氏病的治疗中有益。 [参考：22]

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