The sequence of molecular events that turns the states of normal αS into pathological forms over time is a complex topic, but environmental factors, excess αS, missense mutations in αS, and other genetic risk factors influence the conversion of “good” αS into “bad”. Our long-term goal is to understand the normal αS biology and test how its functions are compromised under pathological states by exploiting factors that accelerate αS dyshomeostasis. We then seek to convert “bad αS” back to “good αS”.