Insitute of Neurodegenerative Diseases, Université Victor Ségalen-Bordeaux II, Centre National de la Recherche Scientifique, Bordeaux, France.
Mov Disord. 2011 May;26(6):993-1002. doi: 10.1002/mds.23696.
Parkinson's disease is a neurodegenerative disorder whose cardinal manifestations are due primarily to a profound deficit in brain dopamine. Since the 1980s, several therapeutic strategies have been discovered to treat the symptoms of this neurological disorder, but as of yet, none halts or retards the neurodegenerative process. In an attempt to shed light on the neurobiology of Parkinson's disease, a number of experimental models have been developed, especially during the last 25 years. They come essentially in 3 flavors: pharmacological (eg, reserpine), toxic (eg, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), and genetic (eg, transgenic synuclein mice). These models can also be recast as etiologic, pathogenic, and symptomatic/pathophysiologic, as each may contribute to our understanding of the cause, the mechanisms, and the treatment of Parkinson's disease. In this review, we will discuss the question of Parkinson's disease models, starting from the period when this journal was born to today. During this journey of 25 years, we will discuss both the significant contributions of the Parkinson's disease models and hurdles that remain to be overcome to one day cure this neurological disease.
帕金森病是一种神经退行性疾病，其主要表现主要归因于大脑多巴胺的严重缺乏。自 20 世纪 80 年代以来，已经发现了几种治疗这种神经紊乱症状的治疗策略，但到目前为止，没有一种策略可以阻止或延缓神经退行性过程。为了深入了解帕金森病的神经生物学，已经开发了许多实验模型，尤其是在过去的 25 年中。它们主要有 3 种类型：药理学（例如利血平）、毒性（例如 1-甲基-4-苯基-1,2,3,6-四氢吡啶）和遗传（例如转基因突触核蛋白小鼠）。这些模型也可以被重新定义为病因学、发病机制和症状/病理生理学，因为每种模型都可能有助于我们了解帕金森病的病因、机制和治疗方法。在这篇综述中，我们将从本刊创刊开始讨论帕金森病模型的问题，一直到今天。在这 25 年的历程中，我们将讨论帕金森病模型的重要贡献，以及仍然存在的障碍，以期有一天能够治愈这种神经疾病。
