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Parkinson’s Disease (PD) is a complex and multifactorial disorder of both idiopathic and genetic origin. Thus far, more than 20 geneshave been linked to familial forms of PD. Two of these genes encode for ATP13A2 and alpha-synuclein (asyn), proteins that seemto be members of a common network in both physiological and disease conditions. Thus, two different hypotheses have emergedsupporting a role of ATP13A2 and asyn in metal homeostasis or in autophagy. Interestingly, an appealing theory might combinethese two cellular pathways. Here we review the novel findings in the interaction between these two proteins and debate the excitingroads still ahead.