Fig. 2
Boxplot diagrams representing the distribution of soluble (Sol.), dispersible (Disp.), membrane-associated (Memb. ass.), and plaque-associated (Plaq. Ass.) Aβ (a, d, g, j, m), AβN3pE (b, e, h, k, n), and AβpSer8 levels (c, f, i, l, o) in relation to the phase of Aβ plaque distribution (Aβ phase; a-c), the AβMTL phase (d-f), the A-score (g-i), the CAA stages (j-l) and the CAA severity (m-o) in cohort 1. The correlation for these three different forms of Aβ was best for Aβ detected with antibodies against non-modified forms of Aβ (Spearman correlation analysis: r = 0.603–0.809) followed by AβN3pE (Spearman correlation analysis: r = 0.572–0.756) whereas AβpSer8 was not detectable in soluble Aβ aggregates. Dispersible, membrane-associated and plaque-associated AβpSer8 showed a week correlation with the Aβ phases (Spearman correlation analysis: r = 0.324–0.556) due to the fact that it was seen only in Aβ phases 4 and 5 but not earlier, except for single cases. Increased levels of Aβ and AβN3pE were found already in cases without CAA (m, n). Cases with CAA showed high levels of soluble, dispersible, membrane-associated, and plaque-associated Aβ and AβN3pE in all stage and severity degrees of CAA. Only the presence of AβpSer8 was restricted to cases with CAA. The detailed correlation analysis is provided in Additional file 1: Table S5a