Effects of arsenic treatment on Aβ aggregation and Aβ toxicity in the C. elegans model of Alzheimer’s disease

Environmental stressors influence cellular communication networks that maintain proteostasis and organismal homeostasis. Heavy metals, as common environmental pollutants, can disrupt these processes through oxidative and proteotoxic stress, thereby contributing to protein misfolding and neurodegenerative disease progression. However, how environmental exposure during development shapes later proteotoxic outcomes remains incompletely understood. My research investigates the impact of developmental heavy metal exposure on neurodegeneration-associated protein aggregation using Caenorhabditis elegans models expressing human amyloid beta (Aβ₁–₄₂) and polyglutamine proteins. By combining phenotypic analysis with molecular and proteomic approaches, I aim to understand how environmental stress influences aggregation behaviour and stress adaptation mechanisms. Our findings indicate that environmental exposure can differentially affect proteotoxic phenotypes depending on the aggregation context, suggesting distinct cellular responses to different protein species. These observations further point toward alterations in stress adaptation and proteostasis-related pathways beyond simple changes in aggregate abundance. This work contributes to understanding how environmental signals are translated into organismal stress responses and adaptive processes. In the broader context of microbial communication, these findings relate to how environmental conditions shape cellular decision-making and interlinked stress-response networks across biological systems.

PhD start: 04/01/2020