Hirsch E C
INSERM U679, Hôpital de la Salpêtrière, Université Pierre et Marie Curie-Paris 6, Paris, France.
J Neural Transm Suppl. 2006(70):255-60. doi: 10.1007/978-3-211-45295-0_39.
Ideally, animal models of Parkinson's should reproduce the clinical manifestation of the disease, a loss of some but not all dopaminergic neurons, a loss of some non dopaminergic neurons and alpha-synuclein positive inclusions resembling Lewy bodies. There are at least three ways to develop animal models of PD. The first two are based on the etiology of the disease and consist in 1) reproducing in animals the mutations seen in inherited forms of PD; 2) intoxicating animals with putative environmental toxins causing PD. The last method currently used, which is not exclusive of the first two, is to try to reproduce the molecular or biochemical changes seen post-mortem in the brain of patients with PD. In this review we discuss the advantages and the drawbacks in term of neuroprotection of the currently used models.
理想情况下,帕金森病的动物模型应重现该疾病的临床表现,即部分而非全部多巴胺能神经元丧失、部分非多巴胺能神经元丧失以及出现类似路易小体的α-突触核蛋白阳性包涵体。至少有三种方法可用于建立帕金森病的动物模型。前两种方法基于疾病的病因,包括:1)在动物中重现遗传性帕金森病中出现的突变;2)用假定的环境毒素使动物中毒从而引发帕金森病。目前使用的最后一种方法并非独立于前两种,而是试图重现帕金森病患者死后大脑中观察到的分子或生化变化。在本综述中,我们将从神经保护的角度讨论当前所用模型的优缺点。