Fiber Tracts Anomalies in APPxPS1 Transgenic Mice Modeling Alzheimer's Disease

Figure 6

Aβ pathology in APPxPS1 mice. 24-month-old APPxPS1 mice display heavy cortical amyloid burden as evidenced by Congo red staining (a). Congophilic plaques were also observed in white matter tracts such as the corpus callosum (outlined rectangular area in magnification in (b)) and the anterior commissure (outlined in a and pointed by a black arrow head). In young APPxPS1 mice dense core amyloid plaques were virtually absent but strong Aβ intraneuronal accumulation, as revealed by 4G8 immunostainings, was detected in infragranular cell layers ((c), magnified view in (d)). (e) Biotinylated dextran amine, an anterograde tracer, was injected in the deep layers of the isocortex (left hemisphere) at the locus where Aβ-containing neurons were found in APPxPS1 transgenics. These neurons send their axons through the corpus callosum and cingulum bundle, cross the midline, and innervate the opposite (right) hemisphere. Scale bars: 1000 μm (a), 100 μm ((b), (c), and (d)), and 500 μm (e).