Our lab seeks to understand how intracellular transport and membrane dynamics regulate synaptic function, and how their disruption contributes to neurodegenerative disease. Because defects in these pathways often represent early and actionable events in disease, defining their underlying mechanisms can provide critical insight into pathogenesis and reveal new therapeutic opportunities.
We combine genetically encoded tools with advanced optical and functional approaches to probe and manipulate synaptic biology with high spatial and temporal precision. By targeting specific cell types and pathways, we investigate how synaptic proteins are organized, mobilized, and regulated under physiological conditions, and how these processes break down in disease.
Projects in the lab are centered on the cell biology of synaptic vesicle cycling, protein homeostasis, and intracellular transport in both health and disease. In parallel, we pursue translational efforts that use gene-editing strategies to modulate these pathways in models of Parkinson’s and Alzheimer’s disease, with the goal of developing next-generation, disease-modifying neurotherapeutics.
Research Areas
1. Uncovering the Physiological Roles of α-Synuclein
We investigate the endogenous functions of α-synuclein at the synapse, focusing on its role in regulating synaptic vesicle organization, mobility, and recycling. Our goal is to define how α-synuclein supports synaptic homeostasis under physiological conditions and how these functions are altered in disease.
2. Post-Translational Modifications of Synaptic Proteins in Health and Disease
We study how post-translational modifications (PTMs) regulate the function of synaptic proteins under physiological and pathological conditions. Our work focuses on how modifications such as phosphorylation shape protein interactions, localization, and activity at synapses, and how their dysregulation contributes to synaptic dysfunction and neurodegeneration.
3. Chaperone-Mediated Regulation of Synaptic Health
We explore how molecular chaperones maintain synaptic proteostasis by regulating the folding, trafficking, and turnover of presynaptic proteins. In particular, we investigate how chaperone systems coordinate neurotransmitter synthesis, vesicle loading, and protein quality control, and how these pathways can be leveraged to protect synapses in disease.
4. Lysosome and Autophagy Mechanisms in Synaptic Health and Neurodegeneration
We examine how lysosomal and autophagic pathways preserve synaptic integrity by clearing damaged proteins and organelles. Our research focuses on how these systems function locally at synapses, how they fail in neurodegenerative disease, and how enhancing them may provide therapeutic benefit.