Figure 1.

Aβ, Aβ_N3pE and Aβp_Ser8 loads in the human brain among different Aβ phases. (A–D) Box plot diagrams comparing Aβ loads in the human brain among Aβ phases 0–5. Aβ, Aβ_N3pE and Aβ_pSer8 loads were obtained immunohistochemically in the temporal neocortex (Brodmann area 36) (A), the cingulate gyrus (Brodmann area 24) (B), the putamen (C) and the cerebellar cortex (D) (n = 44). All Aβ, Aβ_N3pE and Aβ_pSer8 loads increased with advancing Aβ phase as dependent variable (linear regression analysis with age and sex as additional covariates: P < 0.05; β: 0.289–0.731), except for the cerebellar Aβ_pSer8 load (linear regression analysis with age and sex as additional covariates: P = 0.233). Presumably non-modified Aβ prevailed over Aβ_N3pE and Aβ_pSer8 in the temporal cortex, cingulate gyrus and putamen [Friedman test corrected for multiple testing (two-sided): P < 0.05]. Aβ_N3pE was here more abundant than Aβ_pSer8 [Friedman test corrected for multiple testing (two-sided): P < 0.05]. In the cerebellar cortex, which was only involved in Aβ pathology in 10 out of 11 Aβ phase 5 cases, presumably non-modified Aβ was more abundant than Aβ_pSer8 [Friedman test corrected for multiple testing (two-sided): P < 0.001] and a trend was observed for more abundant Aβ_N3pE than Aβ_pSer8 [Friedman test corrected for multiple testing (two-sided): P = 0.059; non-corrected P = 0.019]. Box elements: centre line = median; box limits = upper and lower quartiles; whiskers = 1.5× interquartile range; dots/stars = outliers.