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Figure 2 | Molecular Neurodegeneration

Figure 2

From: Vascular and parenchymal amyloid pathology in an Alzheimer disease knock-in mouse model: interplay with cerebral blood flow

Figure 2

Aβ levels and amyloid pathology in APP DSL and APP SL mice. A and B. Sandwich ELISA analysis of Aβ1-40 (Aβ40, A) and Aβ1-42 (Aβ42, B) levels in Triton X100 soluble fractions of young (Y, ~ 6 month), middle (M, 10 ~ 12 month), and old (O, 18 ~ 20 month-double check Result section) of APP DSL and APP SL brain lystates. C and D. Aβ40 (D) and Aβ42 (E) levels in Triton X100 insoluble fractions of the corresponding age groups in A & B. WT: Wild type brain lysate, used as background control. Values of APP SL mice in only the old aged group was shown since the young and middle age groups were at background levels. E. upper panel, Aβ immunostaining using the anti- antibody showing age-dependent increases of parenchymal plaque in APP DSL knock-in mice. F. Fluorescent images demonstrate the consistence between the antibody staining and Thioflavin S (ThioS) staining. G. Quantification of percentage of plaques in whole cortical areas. N = 3 mice/genotype for young and old age group, and n = 5 mice for APP DSL middle age group. ***p < 0.001. Scale bar: 100 μm.

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