Skip to main content
Fig. 4 | Journal of Neuroinflammation

Fig. 4

From: Cu(II) enhances the effect of Alzheimer’s amyloid-β peptide on microglial activation

Fig. 4

Cu(II)-Aβ complex causes indirect, microglia-mediated neurotoxicity. a Cell viability of hippocampal neurons treated with Cu(II)-Aβ1–40 (1–10 μΜ peptide), Aβ1–40, or Cu(II) for 24 h. b Conditioned media (CM) from microglia stimulated with Cu(II)-Aβ1–40 (5 μΜ peptide, 24 h) caused neurotoxicity. Hippocampal neurons were treated with five types of media diluted into the neuronal culture media at indicated percentiles for 24 h. They are (1) media with direct addition of Cu(II)-Aβ1–40 (5 μM peptide), (2) media previously conditioned by unstimulated microglia (con-CM), (3) media previously conditioned by Aβ1–40-stimulated microglia (Aβ-CM), (4) media previously conditioned by Cu(II)-stimulated microglia (Cu-CM), and (5) media previously conditioned by Cu(II)-Aβ1–40-stimulated microglia (Cu-Aβ-CM). Data are expressed as the means ± SEM of at least three independent experiments. Significance was tested by one-way or two-way ANOVA followed by Bonferroni post-test comparisons. *P < 0.05, **P < 0.01 vs control (a) or con-CM (b); # P < 0.05 vs Aβ-Cu-CM. c Cu(II)-Aβ1–40 caused indirect, microglia-mediated damage to neuronal dendrites. All CM used were diluted at 50 % into the neuronal culture media. The control group was treated with solvent only. Neuronal dendrites were observed by immunostaining for MAP2 (green)

Back to article page