Magali Colombat

Accelerated Apolipoprotein A-II senile amyloidosis in a PAI-1 (plasminogen activator inhibitor 1) knock-out 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.

Molecular basis for a novel systemic form of human hereditary apoA-I amyloidosis with vision loss

The paper identifies a novel form of hereditary apoA-I amyloidosis caused by Glu34Lys mutation, revealing structural changes that lead to amyloid formation and vision loss.