Files
Abstract
Parkinson's disease (PD) is a progressive neurodegenerative disorder for which there are currently no treatments to slow, halt, or reverse the disease process. The disease is defined by the accumulation of the protein alpha-synuclein into aggregates known as Lewy inclusions, but how these aggregates initiate and propagate to various locations throughout the brain is unknown. To develop targeted disease modifying therapies, it is important to understand how aggregated forms of alpha-synuclein are transported throughout the nervous system and to determine the effect aggregation of alpha-synuclein has on specific cell types and specific behaviors. The hypotheses of this research are that alpha-synuclein aggregates propagate through neuroanatomically connected pathways and that induction of Lewy pathology results in behavioral deficits.