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Fig. 3 | Acta Neuropathologica Communications

Fig. 3

From: Mutation-induced loss of APP function causes GABAergic depletion in recessive familial Alzheimer’s disease: analysis of Osaka mutation-knockin mice

Fig. 3

Aβ accumulation in OSK-KI mice. Brain sections were stained with anti-Aβ42 Ter42 (a), anti-Aβ N-terminus β001 (b) and Aβ oligomer-specific 11A1 antibodies (c). Photographs were taken from the posterior parietal association area (PPtA) of the cerebral cortex (CTX), hippocampal CA3 region (CA3), dentate gyrus (DG), and entorhinal cortex (EC). Arrowheads indicate Aβ accumulated within neurons. Scale bar = 30 μm. (d) Brain homogenates at 4 and 8 months were separated into TBS-soluble and insoluble (SDS-soluble) fractions and subjected to Aβ42 sandwich ELISA. Each bar represents the mean ± SEM (n = 4 for each group). *p = 0.0391 versus hetero-KI, **p = 0.0255 versus non-KI and = 0.0441 versus hetero-KI. (e) For Aβ oligomers, brain homogenates were subjected to direct ELISA with 11A1 antibody. Each bar represents the mean ± SEM (n = 4 for each group). †p = 0.0001 versus non-KI and = 0.0002 versus hetero-KI. (f) HEK293 cells were transfected with human (h) or mouse (m) APPSW and APPSW/OSK constructs. Three days after transfection, the cells were homogenized and subjected to Western blot to measure APP expression (C40) and actin. Intracellular Aβ were immunoprecipitated using anti-Aβ antibody β001 and subjected to Western blot with the same antibody

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