Monoamine Oxidase Inhibitor (MAO-I)-Mediated Neuroprotection for Treating Parkinson’s Disease
Monoamine Oxidase Inhibitor (MAO-I)-Mediated Neuroprotection for Treating Parkinson’s Disease
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单胺氧化酶抑制剂 (MAO-I) 介导的神经保护治疗帕金森病
DOI：
10.1007/978-3-319-56015-1_238-1
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发表时间：
2020
期刊：
影响因子：
--
通讯作者：
Nagatsu T,Nakashima A
中科院分区：
文献类型：
--
作者：
Shigesaburo Ogawa;Mai Shinkawa;Ryuji Hirase;Taro Tsubomura;Katsuya Iuchi;Setsuko Hara;岩部 真人;Nagatsu T,Nakashima A
单胺氧化酶（MAO）-A和MAO-B催化中枢和外周神经系统中单胺神经递质如多巴胺（DA）、去甲肾上腺素和5-羟色胺的氧化脱氨。帕金森病（Parkinson's disease，PD）是一种与衰老相关的运动障碍，由黑质纹状体DA神经元的变性引起的大脑纹状体中神经递质DA的缺乏引起。在20世纪60年代，L-DOPA，DA的直接前体，其在体内由DA神经元中的酪氨酸通过酪氨酸羟化酶合成，并通过芳香族L-氨基酸脱羧酶转化为DA，被引入以治疗纹状体中的这种DA缺乏症。除了L-DOPA作为治疗之外，自20世纪70年代以来，已经使用MAO-B抑制剂（MAO-B-Is），首先是司来吉兰（L-（-）-丙炔苯丙胺），然后是雷沙吉兰，最近是沙非酰胺，通过防止DA降解作为PD的有效治疗。此外，已经证明用MAO-B-I、司来吉兰、雷沙吉兰或沙非酰胺的单药治疗在早期PD的情况下是有效的。积累的数据表明，由于可能与或可能不与MAO抑制相关的几种机制，MAO-B-Is也可能具有神经保护功效。DA氧化和错误折叠的α-突触核蛋白寡聚体的形成可能与线粒体、自噬-溶酶体系统和泛素-蛋白酶体系统的功能障碍有关，导致PD中的DA神经元死亡;并且MAO-I可能阻止这些过程以提供神经保护。然而，许多临床和基础研究表明，但尚未令人信服地证明，单胺氧化酶-I在PD中的神经保护作用。在PD发病前几十年给予MAO-B-I是否可以预防基于神经保护的PD的发生，如果是这样，还有待于证实所涉及的分子机制。
Monoamine oxidases (MAO)-A andMAO-B catalyze the oxidative deamination of monoamine neurotransmitters, such as dopamine (DA), noradrenaline, and serotonin, in the central and peripheral nervous system. Parkinson’s disease (PD) is an aging-related movement disorder, caused by a deficiency of the neurotransmitter DA in the striatum of the brain, caused by degeneration of the nigrostriatal DA neurons. During the1960s, L-DOPA, a direct precursor of DA, which is synthesized in vivo from tyrosine in DA neurons by tyrosine hydroxylase and is converted to DA by aromatic L-amino acid decarboxylase, was introduced to treat this DA deficiency in the striatum. In addition to L-DOPA as a treatment, MAO-B inhibitors (MAO-B-Is) have been used since the 1970s, first selegiline (L-(-)-deprenyl), then rasagiline, and more recently safinamide, as an effective therapy for PD by preventing the degradation of DA. Furthermore, monotherapy with MAO-B-I, selegiline, rasagiline, or safinamide has been proved to be effective in the case of early PD. Accumulating data suggest that MAO-B-Is may also have neuroprotective efficacy due to several mechanisms that may or may not be related to MAO inhibition. DA oxidation and formation of misfolded α-synuclein oligomers may be linked to dysfunctions of mitochondria, the autophagy-lysosomal system, and ubiquitin-proteasome system, resulting in DA neuron death in PD; and MAO-I may prevent these processes to afford neuroprotection. However, many clinical and basic studies have suggested, but not yet convincingly proved, neuroprotective effects of MAO-I in PD. It remains to be proved if the administration of MAO-B-I several decades before the onset of PD could prevent the occurrence of PD based on neuroprotection and, if so, to confirm the molecular mechanism involved.
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勘误表：雷沙吉兰和司来吉兰治疗帕金森病的疗效：一项为期 3 年的头对头回顾性病例对照研究
影响因子：
6
作者：
E. Cereda;R. Cilia;M. Canesi;S. Tesei;C. Mariani;A. Zecchinelli;G. Pezzoli
通讯作者：
G. Pezzoli
影响因子：
3.3
作者：
BIRKMAYER, W;RIEDERER, P;LINAUER, W
通讯作者：
LINAUER, W
司来吉兰作为帕金森病的主要治疗药物——一项长期双盲研究
影响因子：
3.5
作者：
V. Myllylä;K. Sotaniemi;P. Hakulinen;O. Mäki‐lkola;E. Heinonen
通讯作者：
E. Heinonen
丙肾上腺素和去甲司来吉兰可保护中脑神经元免受谷胱甘肽消耗引起的毒性。
DOI：
--
发表时间：
1998
期刊：
The Journal of pharmacology and experimental therapeutics.
影响因子：
--
作者：
Mytilineou,C;Leonardi,EK;Radcliffe,P;Heinonen,EH;Han,SK;Werner,P;Cohen,G;Olanow,CW
通讯作者：
Olanow,CW
影响因子：
2.9
作者：
M. Naoi;W. Maruyama;P. Dostert;Y. Hashizume;D. Nakahara;Tsutomu Takahashi;M. Ota
通讯作者：
M. Naoi;W. Maruyama;P. Dostert;Y. Hashizume;D. Nakahara;Tsutomu Takahashi;M. Ota