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. Author manuscript; available in PMC: 2015 Jan 30.
Published in final edited form as: Curr Neurovasc Res. 2013 Nov;10(4):297–303. doi: 10.2174/15672026113109990022

Fig. (1).

Fig. (1)

(A) Time course of secreted amyloid-precursor proteins APP-β release with (open circles) and without (filled circles) recombinant BACE1 (β-secretase) measured after 2.5 hours, 1-3-6 days. Values are mean±SEM pg/ml*25 μg (n=5). (B) When Alzheimers disease (AD) platelet extacts (25 μg) were incubated without (−) or with 100 or 10 μg/ml BACE1 inhibitor (INH100, INH10), the increase in sAPP-β release was significantly blocked by 100 μ/ml inhibitor. The respective amount of DMSO served as a control. (C) BACE1was significantly enhanced in AD platelets but not in platelets of young controls (COy) or patients with mild cognitive impairment (MCI) compared to old controls (COo). Values are pg/ml*25/μ*150 min (A,B) or mean±SEM pg/mg protein (C); values in parenthesis give the number of n. Statistical analysis was performed by students T-test (A) or one way ANOVA (B,C) with a subsequent Fisher LSD posthoc test (*p<0.05; *** p<0.001). (D) Western Blot analysis of platelet controls (CO) or AD extracts shows APP like immunore activity at approx. 130 and (110/106) kDa. Actin serves as an internal control as seen as a band at approx. 40 kDa. Platelet extracts incubated for 2.5hr at 37°C did not differ from controls, while the APP bands markedly disappeared after incubation with BACE1 overnight at 37°C.