Amyloid plaque deposits composed primarily of Aβ peptides play an important role in the pathology of AD.[33] Plasmin, one of the proteases, is known for its role in regulating Aβ levels.[34] Plasmin formation is mediated by plasminogen activators (tPA and uPA) that cleave the plasminogen to the active plasmin. Here, PLAU is linked to Alzheimer disease.