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. Author manuscript; available in PMC: 2015 Aug 26.
Published in final edited form as: J Alzheimers Dis. 2009;17(4):817–825. doi: 10.3233/JAD-2009-1098

Figure 3.

Figure 3

NDEA treatment causes AD-type molecular abnormalities. Post-mitotic rat cerebellar granule neurons were treated with 0–250 μg/ml NDEA for 48 h. We used cellular ELISAs to measure immunoreactivity corresponding to: (A) Tau; (B) phospho-Tau (p-Tau); (C) amyloid beta precursor protein (AβPP); (D) AβPP-Aβ; (E) ubiquitin; (F) and β-actin. Immunoreactivity was detected with the horseradish peroxidase conjugated Amplex Red soluble fluorophore and quantified in an M-5 Spectromax microplate reader (FLU=fluorescence light units) with results normalized to H33342 fluorescence. Each data point reflects the mean ± S.E.M. for 16 replicate cultures. P-values correspond to levels of significance for dose-effect increasing or decreasing linear trends. Asterisks indicate values that significantly differ from control by ANOVA (P<0.05 or better).