Figure 2

Frontal cortical beta-amyloid (Aβ) neuropathology in dementia pugilistica (DP) as compared to that of Alzheimer’s disease (AD) and nondemented control cases. Aβ1-16 immunostaining illustrates primarily diffuse plaque and extracellular neurofibrillary tangle (NFT) labeling in the DP case (A) as compared to the extensive plaque labeling seen in the frontotemporal dementia (FTD)-­AD case (B), and the typical AD case (C), but is absent in the control case (D). Aβ1-42 immunostaining in the DP case (E), the FTD-AD case (F), the typical AD case (G), and the control (H), was similar to that observed with immunolabeling for Aβ1-16. Less Aβ1-40 immunolabeling was observed in the DP case (I), with deposits being primarily seen within diffuse plaques and on extracellular NFTs. In comparison, Aβ1-40 was observed in plaques in the FTD-AD case (J), and primarily within neuritic plaque cores and associated with blood vessels in the typical AD case (K), and was absent in the control case (L; scale bar = 500 μm). From Saing et al.[5] with permission.