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Parkinson’s disease (PD) is a complex chronic neurodegenerative disease of unknown etiology. A conceptual framework for all chronic diseases involves a series of channels or pathways (aging, genetic, environment, oxidative stress, mitochondrial damage, protein aggregation, etc.) and their interactions. Those channels with specificities may explain the ‘developmental’ program that through transcriptional reprogramming results in stressed dopamine neurons that eventually become dysfunctional or die, giving rise to the clinical manifestations of PD. In Chapter 2 we review the molecular mechanisms of those channels that may be implicated in the pathogenesis of PD and the pathophysiology of the disease based on the anatomo‐physiological complexity of the basal ganglia. This illustrates that understanding the molecular mechanisms of a disease may not be enough, or we have to reach an adequate system level to understand the disease process. Finally, we suggest that common therapies used for the treatment of other chronic diseases may be useful for the treatment (or help to advance the understanding) of PD, as well as new targets for new therapies that may be useful in the prevention of, or to stop the progression of, PD and other synucleinopathies.

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