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. Author manuscript; available in PMC: 2006 Feb 20.
Published in final edited form as: Neuron. 2005 Jul 21;47(2):191–199. doi: 10.1016/j.neuron.2005.06.030

Figure 5.

Figure 5.

Enhanced Pathology in BRI-Aβ42 × Tg2576 Bigenic Mice Transgenic mice expressing both BRI-Aβ42 and mutant APPswe(Tg2576) have enhanced senile plaque pathology in the forebrain compared with their singly transgenic littermates and significantly elevated insoluble Aβ levels in the forebrain and hindbrain. Entorhinal/piriform cortex of 14.5-month-old BRI-Aβ42A mouse (A), 14.5-month-old Tg2576 (B), 14.5-month-old BRI-Aβ42 × Tg2576 bigenic mouse (C) immunostained with anti-total Aβ (33.1.1). All mice were littermates. FA Aβ levels in the forebrain (D) and hindbrain (E) of an aging series of bigenic BRI-Aβ/Tg2576 compared with their single transgenic littermates. Scale bars: 300 μm (A—C).