Scheller Dieter, Chan Piu, Li Qin, Wu Tao, Zhang Renling, Guan Le, Ravenscroft Paula, Guigoni Celine, Crossman Alan R, Hill Michael, Bezard Erwan
SCHWARZ BIOSCIENCES GmbH, Alfred-Nobel Strasse 10, Monheim, Germany.
Exp Neurol. 2007 Feb;203(2):415-22. doi: 10.1016/j.expneurol.2006.08.026. Epub 2006 Oct 12.
Clinical DA agonist monotherapy trials, which used in vivo imaging of the DA transporter (DAT) to assess the rate of progression of nigrostriatal degeneration, have failed to demonstrate consistent evidence for neuroprotection. The present study aims at reconciling these experimental and clinical data by testing the protective property of the continuously delivered D3/D2/D1 dopamine receptor agonist rotigotine. Using a progressive 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned (MPTP) macaque model that mimics the progression of Parkinson's disease in vivo ([99mTc]-TRODAT-1 single photon emission computed tomography (SPECT)) and ex vivo ([125I]-nortropane DAT labelling) endpoints were evaluated. After 38 days of treatment followed by two weeks of washout, rotigotine-treated animals were significantly less parkinsonian than the vehicle-treated ones. Such behavioural difference is the consequence of a partial protection of the DA terminals as could be confirmed by ex vivo DAT labelling. However, the protection of nerve terminals was not detected using SPECT. The data suggest that rotigotine exerts partial protection but that conventional imaging would not be able to identify such protection.
临床多巴胺激动剂单药治疗试验利用多巴胺转运体(DAT)的体内成像来评估黑质纹状体变性的进展速度,但未能证明神经保护作用的一致证据。本研究旨在通过测试持续给药的D3/D2/D1多巴胺受体激动剂罗替戈汀的保护特性,来协调这些实验和临床数据。使用一种渐进性1-甲基-4-苯基-1,2,3,6-四氢吡啶损伤(MPTP)猕猴模型,该模型模拟帕金森病在体内的进展情况(通过[99mTc]-TRODAT-1单光子发射计算机断层扫描(SPECT)),并在体外评估(通过[125I]-去甲托烷DAT标记)终点。经过38天的治疗,随后停药两周,接受罗替戈汀治疗的动物比接受赋形剂治疗的动物帕金森症状明显减轻。这种行为差异是多巴胺能终末部分保护的结果,这可以通过体外DAT标记得到证实。然而,使用SPECT未检测到神经终末的保护作用。数据表明,罗替戈汀发挥了部分保护作用,但传统成像无法识别这种保护作用。