Mitigation of Amyloid Protein Fibrillation and Cellular Interaction with Nanostructures

Proteins and peptides can aggregate and misfold into long twisted fibrils called amyloids. This phenomenon leads to toxicity and cell degeneration and contributes to a range of human diseases, including type 2 diabetes, Alzheimer’s and Parkinson’s disease. This thesis is focused on understanding the relationship between amyloidosis and immunogenicity, as well as the role of nanoparticle inhibitors in mitigating protein fibrillation, toxicity and dysregulation that are associated with amyloid diseases, in vitro, in silico and in vivo. This research sheds new light on the mechanisms of amyloidosis and facilitates the development of nanomedicines against debilitating amyloid diseases.