I’m a neuroscientist interested in exploring mechanisms of long-term memory formation and disruption in health and disease.

I’m currently a postdoctoral research fellow in the lab of Dr. Sabrina Simoes at Columbia University. My research focuses on the molecular and cellular mechanisms by which endosomal trafficking dysfunction contributes to memory impairment and Alzheimer’s disease (AD) pathogenesis. I am particularly interested in identifying early biomarkers of endo-lysosomal dysfunction in brain-derived extracellular vesicles and in elucidating the mechanistic links between disrupted intracellular trafficking, synaptic vulnerability, and memory deficits. My current work combines in vivo behavioral paradigms, primary neuronal culture, high-resolution imaging, and quantitative proteomics, with a focus on genetic models of AD and Down syndrome, a population with near-universal development of AD pathology in adulthood.

I completed my PhD in the Department of Physiology at the University of Toronto under the supervision of Dr. Zhong-Ping Feng, where I investigated the molecular basis of long-term memory consolidation using the invertebrate model Lymnaea stagnalis. My doctoral research integrated behavioral phenotyping, single-cell electrophysiology, and transcriptome-guided bottom-up proteomics to uncover conserved molecular signatures of memory formation. This work led to the identification of several novel candidate proteins regulating long-term memory consolidation, and contributed to the further development of Lymnaea as a useful model for systems-level studies of memory-related proteomic changes.

As I transition into mammalian and disease-relevant systems, I aim to bridge basic mechanisms of memory consolidation with the molecular pathogenesis of neurodegenerative disease. My long-term objective is to establish an independent research program that integrates molecular neuroscience, behavior, and multi-omics to investigate how memory-encoding circuits are disrupted in aging and Alzheimer’s disease. I am particularly interested in whether endosomal dysfunction within memory-associated neuronal ensembles underlies vulnerability to cognitive decline.