Plasminogen activator inhibitor 1 (PAI-1) and tissue plasminogen activator (tPA) are involved in the complications of type 2 diabetes mellitus (T2DM) and early pathology of Alzheimer's disease.
These results suggest reciprocal feedback influences between tPA, PAI-1 and Aβ during aging and amyloid pathogenesis in AD brain; tPA-mediated plasmin activity is declined throughout the brain causing Aβ deposition during aging, and the Aβ deposits locally attract the cluster of tPA and/or PAI-1 around their deposits to competitively determine tPA/plasmin-mediated Aβ proteolysis.
The activity of both plasmin and tissue plasminogen activator are reduced in Alzheimer's disease brain, while the tissue plasminogen activator inhibitor neuroserpin is up-regulated.