TY -的T1 -司立吉林单一疗法治疗帕金森病JF -神经学乔-神经病学SP - 196 LP - 199年代做- 10.1212 / WNL.47.6_Suppl_首页3.196S六世- 47 - 6,85盟威廉·c·科勒Y1 - 1996/12/01 UR - //www.ez-admanager.com/content/47/6_Suppl_3/196S.abstract N2 -帕金森病(PD)的神经化学基础是纹状体多巴胺的减少。代谢的主要酶多巴胺在大脑中单胺氧化酶(MAO)。因此,一个合乎逻辑的方法是抑制毛为了保护内源性多巴胺。非选择性,毛不可逆抑制剂作为单一疗法显示最小PD的临床效果。[1]当这些药物结合左旋多巴,发生有益的影响;然而,在血压结果显著上升(酪胺或“奶酪”效应)。[2 - 4]因此,这种组合疗法已被抛弃。毛已经被发现在两种形式存在,最初由他们对抑制药物的敏感性定义clorgyline,一种更敏感型B[5]毛泽东发现大脑中主要是B型,当毛泽东在肠道主要类型A[6]脑部多巴胺可能主要代谢缺氧,但可能intraneuronal的重要性是在大脑中应该考虑。毛的一个新类抑制剂开发选择性[7,8],缺氧的不可逆抑制剂,从而能够保持内生和外生没有是多巴胺介导的“奶酪”效应。这些药物之一,isopropylmethylpropargylamine盐酸,称为deprenyl或司立吉林,经历了进一步的临床开发。 Since deprenyl blocks MAO-B in the brain, it was thought that endogenous dopamine could be increased, resulting in symptomatic improvement. Bhatin et al. [9] studied deprenyl in 20 PD patients who were in the early phase of the disease and initially noted improvement in clinical scores, followed by subsequent worsening. They concluded that deprenyl may have a short-lasting symptomatic effect. The French selegiline multicenter trial [10] investigated whether the disability of de novo patients with parkinsonism could be improved during the first 3 months by deprenyl monotherapy (10 mg/day). The double-blind, randomized, placebo-controlled trial … ER -