Fig. 6

Progressive accumulation of Aβ deposits is not topographically parallel to tau deposits. a-g Representative midbrain (a-d, case 23, SC) and pontine section (e-g, case 23, pontine nucleus), stained with Aβ/DAB. As Iseki et al. have described [27], Aβ deposits showed various morphologies; e.g., amyloid plaques type 1 (a, e, ‘amyloid core with surrounding processes’), type 2 (b, f, ‘amorphous amyloid with surrounding processes’), and type 3 (c, g, ‘ill-defined aggregation of the fine processes’). Fleecy amyloid deposits [50] surrounded a capillary wall (d). Scale bar = 20 μm. (h) Box plots of the cortical NFT stages in different degrees of local Aβ deposition at the midbrain (left panel) and pons (right panel). i Percentages of the cases with Aβ deposition at the midbrain (blue) and pons (orange) with advancing NFT stages (left panel) and CERAD neuritic plaque score (right panel). j, k DAB staining of AT8 (j) and Aβ (k) immunohistochemistry at the LC (case 21) showed absence of Aβ in the presence of tau deposition in this case. Bar = 200 μm. l-n Aβ/DAB-stained sections of the midbrain (l, m, cases 10 and 23, respectively) and pons (n, case 22) showed dorsal predilection of Aβ deposition at the PAG (l, solid arrow), which was dissociated from the ventral predilection of tau deposition (Fig. 5a, b, open arrows). The SC (l, m, open arrowheads) showed abundant Aβ deposition. The subnucleus medialis (l, m, solid arrowheads) was free of Aβ depositions. Bar = 2 mm. LC (n, open arrow), MRN (n, solid arrowhead) and reticular formation (n) showed involvement with Aβ deposition. Lesions in the DRN (n, open arrowhead) were only sparsely detected. Bar = 2 mm