Abstract
Alpha-synuclein (α-syn) is a presynaptic and nuclear protein that has been inextricably linked to Parkinson’s disease (PD). It regulates the presynaptic activities of neurons, but its aggregation and spreading have been associated with a group of diseases termed synucleinopathies. Here, we examined the commonly held view that α-syn caused disease and explored the concept that α-syn aggregation may be a consequence of pathobiology. Future therapies may need to encompass α-syn both a cause and consequence of the disease process.
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