prab10 synuclein vglut merged
The goal of the Volpicelli-Daley lab is to stop the progression of Parkinson's Disease and Lewy Body Dementias by preventing the formation and spread of α-synuclein aggregates

Parkinson’s disease (PD) and Lewy body dementias (LBDs), collectively known as synucleinopathies,
impact over 2 million people in the United States. Synucleinopathies are characterized by aggregates in neurons called Lewy Bodies and Lewy neurites, composed mostly of α-synuclein. PD is well known for its characteristic motor defects, but it is becoming more appreciated that the nonmotor symptoms, including cognitive impairments contribute greatly to reduced quality of life for both the patient and caregiver. Up to 80% of PD patients develop cognitive symptoms. In addition, LBDs are the second most common cognitive disorder after Alzheimer's disease. Lewy pathology is also found in 50% of brains from Alzheimer's disease patients. There are no treatments to stop the progression of these neurodegenerative diseases.  

We use live imaging of neurons, super-resolution expansion microscopy, and biochemical techniques to determine how leucine-rich repeat kinase 2, the most common genetic cause of PD, influences the synaptic localization of alpha-synuclein. We are also using mouse genetic models to determine which genes implicated in PD and LBD impact formation of alpha-synuclein inclusions in brain regions important for cognition. The lab is also determining  the consequences of early formation of these aggregates on neuronal structure, function and connectivity.  Finally, we collaborate with pharma and biotech to find thereapeutic strategies to prevent the formation of these aggregates throughout the central nervous system.