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. Author manuscript; available in PMC: 2011 Feb 28.
Published in final edited form as: Acta Neuropathol. 2009 Aug 19;119(2):221–233. doi: 10.1007/s00401-009-0583-3

Fig. 1. Aβ and tau pathology in the superior temporal gyrus of the PIB-refractory Alzheimer’s case AD1.

Fig. 1

(a) Antibody 6E10-immunoreactive senile plaques (two denoted by arrows) and large-vessel CAA (black arrowhead). (b) Antibody CP13-immunoreactive, intra-somatal neurofibrillary tangles (two denoted by arrowheads) and abundant neuropil threads. (c) Ultrastructure of amyloid fibrils in the periphery of a senile plaque. (d) Ultrastructure of a bundle of paired helical filaments (marked by two arrowheads). Case AD1 had significant CAA, and the senile plaques sometimes showed diminished immunostaining in the central region (right-hand arrow in a), but otherwise the histopathology did not differ remarkably from that of the other AD cases. Bar = 100μm in a and b and 200nm in c and d).