Sébastien Bender

This paper characterizes AT-03, a novel fusion protein that binds and removes various amyloid types, showing therapeutic efficacy in a mouse model.

This study shows PAI-1 knockout mice develop systemic AApoA-II amyloidosis at intermediate age, with amyloid deposits in multiple organs and urinary albumin as a biomarker, highlighting potential risks of PAI-1 inhibition in amyloidosis.

This paper develops a mouse model of cardiac AL amyloidosis that reproduces human disease features, including amyloid deposits and cardiac dysfunction, and identifies a role for partial LC degradation in fibril formation.

This study develops a mouse model of light chain deposition disease, showing that pathogenic light chains cause glomerulosclerosis and kidney failure, and identifies potential therapeutic targets.