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. 2013 Nov 20;8(11):e80700. doi: 10.1371/journal.pone.0080700

Figure 3. APOE ε4 allele accelerates disease progression and increases soluble Aβ42 levels in the temporal cortex in a dose-dependent manner.

Figure 3

(A) APOE ε4 carriers are overrepresented in the moderate and severe groups (p<0.001, Pearson χ2, n =  (APOE ε4-/ε4+) mild 31/15; moderate 4/10; severe 4/23). (B) Aβ42-ELISA reveals a gene dose-dependent increase in the soluble Aβ42 levels in the temporal cortex of patients carrying the APOE ε4 allele (***p<0.001, **p<0.01, ANOVA LSD, n =  3/2/36/35/9, APOE genotypes 23/24/33/34/44, respectively). (C) β-secretase activity assay shows a trend towards an increased β-secretase activity in relation to the copy number of APOE ε4 allele (n =  3/2/36/35/9, APOE genotypes 23/24/33/34/44, respectively). (D) The qPCR analysis does not indicate significant changes in APOE mRNA levels in the temporal cortex with respect to the number of APOE ε4 alleles (n = 26/28/6, number of APOE ε4 alleles 0/1/2, respectively). Mean values are indicated in the graphs and each dot represents one individual.