Lopes da Fonseca Tomás, Outeiro Tiago Fleming
Department of Neurodegeneration and Restorative Research, Center for Nanoscale Microscopy and Molecular Physiology of the Brain, University Medical Center Göttingen, 37073 Göttingen, Germany. ; Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Portugal.
Exp Neurobiol. 2014 Dec;23(4):314-23. doi: 10.5607/en.2014.23.4.314. Epub 2014 Dec 12.
Parkinson's Disease (PD) is a complex and multifactorial disorder of both idiopathic and genetic origin. Thus far, more than 20 genes have been linked to familial forms of PD. Two of these genes encode for ATP13A2 and alpha-synuclein (asyn), proteins that seem to be members of a common network in both physiological and disease conditions. Thus, two different hypotheses have emerged supporting a role of ATP13A2 and asyn in metal homeostasis or in autophagy. Interestingly, an appealing theory might combine these two cellular pathways. Here we review the novel findings in the interaction between these two proteins and debate the exciting roads still ahead.
帕金森病（PD）是一种起源于特发性和遗传性的复杂多因素疾病。迄今为止，已有20多个基因与家族性帕金森病相关。其中两个基因编码ATP13A2和α-突触核蛋白（α-syn），这两种蛋白质在生理和疾病状态下似乎都是一个共同网络的成员。因此，出现了两种不同的假说，支持ATP13A2和α-syn在金属稳态或自噬中的作用。有趣的是，一个引人注目的理论可能会将这两条细胞途径结合起来。在这里，我们回顾了这两种蛋白质相互作用的新发现，并探讨了仍有待探索的令人兴奋的研究方向。
