Skip to main content
Fig. 5 | Molecular Neurodegeneration

Fig. 5

From: Amyloid fibril proteomics of AD brains reveals modifiers of aggregation and toxicity

Fig. 5

Mouse and human fibril protein orthologs interact with Aβ42 peptides in vivo and modulate amyloid toxicity in Drosophila. a Biochemical purification workflow and proteomic analysis of amyloid fibril core from transgenic flies expressing Aβ42 in adult brain using the 201Y-Gal4 driver. b Representative WB analysis of the purified material isolated from LacZ control and Aβ42 flies using LOC antibody. c Volcano plot depicting relative abundance of proteins in fibrils isolated from flies expressing Aβ42 in adult brain compared to innocuous LacZ control flies. d Representative eye images of Aβ42-expressing flies carrying the indicated RNAi or overexpression lines for shortlisted genes from the MS analysis. Note that the enhancers do not modify the eye morphology in the absence of Aβ42. Luc-RNAi and UAS-LacZ were used as negative controls against RNAi and overexpression lines, respectively. e Histograms represent the severity scores of the indicated genetic modifiers compared to control flies. Data in e represents mean ± SD; **, p-value < .01; ***, p-value < .001; analyzed with ordinary one-way ANOVA followed by Dunnett’s multiple comparison test. N = 4 biological replicates, 60 flies pooled in each sample (c), 8–15 flies per line (e). Scale bar = 100 µm (d)

Back to article page