Iatrogenic early onset cerebral amyloid angiopathy 30？years after cerebral trauma with neurosurgery: vascular amyloid deposits are made up of both Aβ40 and Aβ42

Neuropathologic findings of the cerebral biopsy. Severe amyloid angiopathy appeared as thickening of the wall of parenchymal arterioles (a, Haematoxylin &Eosin) where amorphous material, fluorescent after thioflavine S treatment, built up (b, thioflavine S). When antibody 4G8 was used (mouse monoclonal, 1:2000, after 80% formic acid for 20？min) that recognizes the different Aβ species (epitope at residues 17–24 of Aβ), immunoreactivity was intense both in parenchymal (c) and leptomeningeal vessels (d). Both the antibody specific for Aβ40 (mouse monoclonal, Covance, 1:1000, after 80% formic acid for 20？min)(e) and that specific for Aβ42 (mouse monoclonal, Covance, 1:500, after 80% formic acid for 20？min)(f) strongly decorated the amyloid-laden vessels. Compact Aβ deposits were present in the neuropil (g, thioflavine S) and were intensely immunolabeled by anti-Aβ42 (not shown) and 4G8 (h), while tau pathology was minimal, appearing as cellular profiles immunopositive for anti-phosphorylated tau antibody AT8 (mouse monoclonal, Biosource, 1:300) often surrounding amyloid laden vessels (i). Immunolabeling was visualized by the Envision Plus/Horseradish Peroxidase System (DakoCytomation) using 3–3′-diaminobenzidine (brown reaction product) as chromogen. Bar in A？=？25？μm (A,B,G,H and I are the same magnification); bar in C？=？100？μm (C,D,E and F are the same magnification