Glia-derived nexin has been found to associate with neuritic plaques in Alzheimer disease [37] and is known to inhibit several serine proteases that cleave at basic residues (the P1 position) including thrombin, urokinase plasminogen activator (uPA) [47], trypsin, plasmin, Factor XIIa, and plasma kallikrein [48,49]. Here, PLG is linked to early-onset autosomal dominant Alzheimer disease.