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Fig. 1 | Acta Neuropathologica Communications

Fig. 1

From: The characterization of AD/PART co-pathology in CJD suggests independent pathogenic mechanisms and no cross-seeding between misfolded Aβ and prion proteins

Fig. 1

Spectrum of Aβ- and tau-positive lesions in representative cases and brain regions. Aβ + lesions (immunostaining with 4G8 antibody, cerebral neocortex a-f, other regions g-l): a Early diffuse Aβ deposits; b Aβ core plaques; a higher magnification of a typical core plaque is shown in the lower left box; c cerebral amyloid angiopathy (CAA) in medium size parenchymal and leptomeningeal vessels and e capillaries; d parenchymal CAA with marked perivascular Aβ deposition; f Aβ deposits with subpial distribution; g dense, coarse Aβ aggregates in the striatum; h diffuse Aβ deposits in the amygdala, and i the CA1 region of the hippocampus; j small focal Aβ deposits in the thalamus, and k periaqueductal grey; l diffuse Aβ deposits in the molecular layer of the cerebellum; cerebellar leptomeningeal CAA is shown in the lower right box. Tau + lesions (immunostaining with AT8 antibody, m-o): m Neurofibrillary tangles (NFT) in the CA1 region of hippocampus of a CJD brain with PART co-pathology; a higher magnification of a globular NFT is shown in the lower left box; n dystrophic tau positive neurites contributing to neuritic plaques in the parahippocampal gyrus; a detail of a neuritic plaques (Gallyas silver staining) is shown in the lower left box; o numerous neuropil threads in the middle temporal gyrus

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