Our lab studies how cells maintain proteostasis—the balance of protein synthesis, folding, and degradation—and how its decline can lead to cellular vulnerability associated with neurodegenerative diseases and aging. We investigate how disturbances in the proteostasis network, the cellular machinery that maintains this balance, promote the aggregation and prion-like spread of disease-associated proteins such as MAPT/Tau and α-synuclein.

A recent focus is on how lysosomal function and lipid metabolism influence the cellular capacity for proteostasis, as the lysosome serves as a key hub connecting protein and lipid homeostasis. We also explore how early-life challenges, including traumatic brain injury (TBI), can lower this capacity and trigger long-term vulnerability of the nervous system.

Using Caenorhabditis elegans and human cell models, we apply advanced microscopy, ribosome profiling, and RNAi- and CRISPR-based genetics to uncover the cellular events that lead to proteostasis collapse and identify pathways that help preserve cellular resilience during aging and disease.

You can find more about our research here.