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Figure 1 | Molecular Neurodegeneration

Figure 1

From: Normal cognition in transgenic BRI2-Aβ mice

Figure 1

Aβ pathology in BRI2-Aβ transgenic mice. Images of the hippocampal region immunostained with an anti-Aβ1-16 antibody (A-C) 12-month-old BRI2-Aβ, (D) 17-month-old non-Tg, (E) 17-month-old BRI2-Aβ1-42 and (F) 4-month-old APP CRND8 mice. (G) Representative 82E1 immunoblots of 4-month-old CRND8 mice and 17-month-old BRI2-Aβ1-42 mice show increased presence of Aβ oligomers (di/tri/tetrameric and higher molecular weight species) as compared to younger 12-month-old BRI2-Aβ and 17-month-old non-Tg mice. The first, control lane includes H4 cell lysate expressing BRI2-C99 fusion protein. A band between 10 and 15 kDa represents C99 peptide. Molecular weight markers are indicated on the left (kD). The lower panel represents the 82E1 blot re-probed with anti-β-actin antibody to depict loading amount (* Bands not characterized). (H-I) RIPA soluble and insoluble Aβ levels in the brains of BRI2-Aβ and CRND8 mice were measured by Aβ ELISA after sequential extraction using RIPA, SDS, and FA (n = 10-15 per genotype). Scale bars (A, D): 250μm, inserts-80μm. Error bars represent s.e.m. For brevity and clarity of presentation, we used shorter labels of BRI2-Aβ lines (BRI2-Aβ40; BRI2-Aβ42; BRI2-Aβ40/42) in the panels of all figures.

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