Skip to main content
. 1999 Jul;155(1):29–37. doi: 10.1016/s0002-9440(10)65095-x

Figure 2.

Figure 2.

AMY 117 IR was not diminished by pre-absorption with Aβ peptide and was less abundant than Aβ42 in old DS brain. a and b: Adjacent 8-μm briefly formalin-fixed, paraffin sections of hippocampus from a 65-year-old DS patient with clinical and neuropathological AD show AβIR (a) was ablated by absorption of Aβ antibody (R1282) with synthetic Aβ1-40 peptide (b). c and d: AMY 117ascIR (c) in serial sections adjacent to those shown in a and b was not diminished by pre-absorption of the AMY 117 antibody with Aβ1-40 peptide (d), indicating that anti-AMY 117 is not an Aβ antibody. Note the close co-occurrence of Aβ and the AMY 117 antigen in virtually all plaques, exemplified by the arrowhead. e and f: Immunoreactivities of Aβ42 (using antibody 21F12) and AMY 117 in adjacent sections approximately 200 μm deeper into the same tissue block shown in a to d indicate that AMY 117 IR occurs only in regions bearing Aβ. Many compacted plaques in the 65-year-old DS brain were labeled by Aβ42 (e) and AMY 117 (f) in hippocampus (DG, dentate gyrus; small arrowheads), parahippocampus (PHC), and temporal cortex (TC). However, AMY 117 IR was absent from Aβ42-rich plaque regions in the subiculum (arrow in e and f) and parahippocampus, in the deep cortical layers and adjacent white matter in temporal cortex (large arrowheads in e and f), and in the subpial layer of cortex (alongside asterisks in e and f). Scale bar, 100 μm (a to d) and 1 mm (e and f).