ABSTRACT
In 1997 and 1998, the protein alpha-synuclein (α-syn) was found to aggregate abnormally in sporadic and familial PD. Many observers have considered this insight into the pathogenesis of PD to be at least as important as the description of MPTP toxicity 15 years earlier. The causes of α-syn aggregation and the details of its relationship to cell loss in PD are the subject of much current work and will continue to cascade out of laboratories for years. But the result so far is a wealth of new etiological and pathogenetic insights, several animal models, and, most important, new potential targets for neuroprotective therapy. This chapter will summarize the current state of knowledge of the role of α-syn in PD.
