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We are particularly interested in Light Chain Amyloidosis, a misfolding disease characterized by the deposition of monoclonal immunoglobulin light chains as amyloid fibrils affecting several organs, causing dysfunction. Understanding the protein misfolding and aggregation mechanisms will help us to understand these diseases and will guide us to design therapeutic strategies to overcome the amyloid phenomenon.
By exploring the role of folding kinetics, misfolding pathways, and stability, it is possible to understand the mechanisms of amyloid formation in light chain amyloidosis, leading to the prediction of the behavior of other amyloid diseases, with the ultimate goal of intervening to prevent progression of the disease.
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