Fig. 3

Quantitative analysis of amyloid β peptide (Aβ) pathology and biochemical studies of the autopsied patients. The images represent the quantitative analysis of Aβ pathology in the autopsied patients (A–D), and concentrations of Aβ40, Aβ42, and Aβ40 + Aβ42, as well as the ratio of Aβ40/Aβ42 in the human brain extracts (E–H) and human brain pellets (I–L). Compared to Aβ, the Aβ40 and Aβ42 loads in the Alzheimer’s disease (AD), cerebral amyloid angiopathy (CAA) and AD + CAA groups, those with less Aβ pathology were much lower (A–C). The CAA scores of the CAA and the AD + CAA groups were higher than those of the AD and the less Aβ groups (D). In the human brain extracts, concentrations of Aβ40 in the CAA and AD + CAA groups were much higher than those in the AD and less Aβ groups, and consequently the concentrations of Aβ40 + Aβ42 in the CAA and AD + CAA groups were also much higher (E and F). The concentrations of Aβ42 in the CAA and AD + CAA groups were also higher than those in the AD and less Aβ groups, but the differences were smaller than for the Aβ40 concentrations (G). The ratio of Aβ40/Aβ42 was Aβ42-dominant in the patients with AD group, while that of the other three groups was Aβ40 dominant (H). In the human brain pellets, the proportion of the concentrations of Aβ40 + Aβ42, Aβ40, and Aβ42, as well as the ratio of Aβ40/Aβ42 among the AD, CAA, AD + CAA, and less Aβ groups were similar to those in the human brain extracts (I–L)