Protein homeostasis or proteostasis is a highly complex and interconnected pathway that regulates the fate of a protein by controlling its biogenesis, folding, trafficking and degradation. Maintenance of proper cellular proteostasis is crucial for ensuring normal development, healthy aging and resistance to environmental stresses. Excessive accumulation of misfolded proteins can disrupt proteostasis and is the cause of many diseases including Alzheimer’s disease, Huntington’s disease and Parkinson’s disease. The cellular mechanisms that are triggered to cope with misfolded proteins are complex and vary depending on the nature of the misfolded protein, its subcellular localization, and the protein degradation pathways employed. A global understanding of the cellular responses could enable the development of novel therapeutic strategies that restore proteostasis and normal health. My current research is focused on modeling protein aggregation disorders in C. elegans and employing innovative, high-throughput strategies to 1) gain a comprehensive understanding of the genetic mechanisms that underlie the disease, and 2) identify therapeutic compounds.