 | Figure 2
Nature Medicine
9, 448 - 452 (2003)
Published online: 17 March 2003; | doi:10.1038/nm840
Neuropathology of human Alzheimer disease after immunization with amyloid- peptide: a case reportJames A.R. Nicoll, David Wilkinson, Clive Holmes, Phil Steart, Hannah Markham
& Roy O. Weller | | | | Figure 2. Distribution of other features of AD pathology in relation to A plaques and association of A with microglia.
a−d, In the immunized case, cortical areas with abundant A plaques (a) (corresponding sections immunostained for tau protein (b)) have plaque-associated dystrophic neurites, neurofibrillary tangles and neuropil threads similar to unimmunized AD. In contrast, cortical areas devoid of A plaques (c) when immunostained for tau protein (d) have neurofibrillary tangles and neuropil threads but lack clusters of dystrophic neurites. Persistence of vascular A (CAA) can be seen in area devoid of A plaques (c; top left). e, Interface between plaque-bearing cortex (right) and area devoid of plaques (left), showing unusual punctate immunoreactivity for A (arrow). f and g, Higher-powered view of an area of parietal neocortex devoid of plaques (f). This area shows punctate immunoreactivity for A, which takes the form of clusters of granules and appears very similar to an adjacent section (g) immunostained with an antibody against lysosomes of phagocytic microglia (CD68). h, Negative control for the corresponding area, without primary antibody.
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