da Fonseca, Tomás LopesOuteiro, Tiago2021-12-022021-12-022014Exp Neurobiol. 2014 Dec;23(4):314-323http://hdl.handle.net/10451/50239© The Korean Society for Brain and Neural Sciences. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.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.engATP13A2Parkinson's DiseaseAlpha-synucleinAutophagyMetal homeostasisjournal article10.5607/en.2014.23.4.3141226-25602093-8144