Fig. 2From: Aβ oligomers trigger necroptosis-mediated neurodegeneration via microglia activation in Alzheimer’s diseaseActivation of RIPK1 and MLKL correlate with soluble Aβ oligomer burden in AD brains. A Western blot analysis of total protein extracts from hippocampal samples using a mix of 6E10 and 82E1 antibodies was performed to determine the Aβ content. B The specific band was quantified by densitometric analysis, and represented in the graphs. C The graph represents the expression levels of Ripk1, Ripk3, and Mlkl in human brain samples from patients at different AD stages (Braak stage II (n = 10), III-IV (n = 9), V-VI (n = 10)). D Dot blots of soluble proteins extracted from postmortem brains of individuals with Braak II (n = 4), Braak III-IV (n = 5), and Braak V-VI (n = 8), probed with the indicated antibodies. E Blots were quantified by densitometric analysis and expressed relative to GAPDH protein, represented in the graph. F, G Association analyses of oligomeric Aβ load and mRNA levels were done by linear regression. H Dot blots of protein extracts from postmortem brains of individuals with Braak II (n = 4), Braak III-IV (n = 5), and Braak V-VI (n = 8), probed with the indicated antibodies. I Blots were quantified by densitometric analysis and expressed relative to GAPDH protein, represented in the graph. J, K Association analyses of oligomeric Aβ load and pMLKL levels were done by linear regression. Data are presented as mean ± S.E.M. Data in B, C, E, and I were analyzed by Kruskal–Wallis test followed by Dunn post-hoc test. Data in F, G, J and K were analyzed by linear regression using Spearman rho-test. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001Back to article page