We explore new strategies for the treatment of Parkinson’s disease (PD) and related synucleinopathies such as Dementia with Lewy bodies (DLB). These diseases are characterized by the aggregation of the protein α-synuclein (αS), an abundant nerve cell component in the brain. With no disease-modifying drugs available, there is a great need for robust models that recapitulate how early changes in the normal maintenance of α-synuclein can lead to these aggregates. Combining cell biology, biochemistry, microscopy, high-content imaging and screening approaches, we want to:

• understand normal αS cell biology,
• define abnormal αS states,
• transform abnormal αS states into screenable phenotypes,
• use the correction of abnormal states as a readout for drug discovery.