PLG and Alzheimer disease: In neuronal cultures, plasmin is capable to cleave, degrade, and reduce both non‐aggregated monomeric and aggregated fibrillar Aβ forms.33, 34, 35 In addition, plasmin protects these neurons from Aβ‐induced cell death33, 34 and enhances clearance of Aβ in AD animal models when PAI‐1 is pharmacologically inhibited.36 These findings suggest that the protease activity of plasmin may be altered during AD.