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. 2007 Jan 17;27(3):627–633. doi: 10.1523/JNEUROSCI.4849-06.2007

Figure 5.

Figure 5.

Steady-state RIPA-soluble brain Aβ levels and plasma Aβ levels in BRI-Aβ40/Tg2576 and BRI-Aβ40/BRI-Aβ42A mice before amyloid deposition. To ensure that there was no change in transgene expression levels or alteration in production of Aβ levels in any of the bigenic mice, RIPA-soluble Aβ levels in forebrain, hindbrain, and plasma were analyzed by Aβ sandwich ELISAs. A–C, The levels of RIPA-soluble Aβ40 and Aβ42 in forebrain (A), hindbrain (B), and plasma (C) of BRI-Aβ40/Tg2576 mice were consistent with an additive sum of Aβ levels from their single transgenic littermates at 8 months of age (p > 0.1). D, E, Bitransgenic BRI-Aβ40/BRI-Aβ42A mice had comparable Aβ40 and Aβ42 levels in hindbrain (D) and plasma (E) compared with BRI-Aβ40 and BRI-Aβ42A single transgenic littermates at 2.5 months of age, respectively (p > 0.1). For statistical analysis, see Materials and Methods.