Clot lysis is delayed through a range of tPA concentrations in the presence of Aβ₄₂ in a dose-dependent manner. Clot formation and lysis were monitored by turbidity assay. (A) Clot formation and lysis were initiated as described in “Clot turbidity analysis” by combining thrombin, fibrinogen, CaCl₂, plasminogen, and 0.15nM, 1.5nM, or 15nM tPA with or without 3μM Aβ₄₂ (0.15nM and 15nM curves not shown because of scale differences). (B) Half-lysis of Aβ clots was significantly longer than for control clots for all concentrations of tPA. (C) Clots were formed as in panel A with 0.5μM, 1.5μM, 3μM Aβ₄₂, or vehicle and 1.5nM tPA. (D) Half-lysis of Aβ clots was significantly delayed in a dose-dependent manner. (E) Preformed clots prepared as described in “Clot turbidity analysis” were overlaid with 50nM tPA. (F) Half-lysis of Aβ clots was significantly longer than control. (G) Clotting and lysis of clots formed as in panel A but with 3μM amylin confirmed by TEM to be fibrillar (inset) did not differ from control. (H) Clots formed as in panel A but with 3μM Aβ_1-28 did not differ from control clots (turbidity plots represent mean of 3 experiments; bar graphs represent mean ± SD of 3 experiments; statistical significance noted as *P < .05, **P < .005, and ***P < .0005).