Immunocytochemical staining with monoclonal antibodies to the beta-protein on tissue sections which have been pretreated with formic acid is not only a very specific but also a highly sensitive method for the detection of amyloid deposits in the brains of Alzheimer's disease victims. We report here a spectrum of morphological appearance of the brain amyloid deposits which are one of the main histopathological correlates of this disorder. Deposits of the beta-protein are not only found in the well-known lesions [congophilic angiopathy and senile (neuritic) plaques] but are also seen under various morphological forms for which the word "plaques" does not appear an appropriate term: amyloid fibrils are found as large areas of diffuse infiltration of the neuropil, as ribbon-like infiltration in the subpial layer of the cerebral cortex, as granular deposits in the white matter, as diffuse deposits in the molecular layer of the cerebellum and the basal ganglia and as star-shaped deposits in the cerebellar Purkinje cell layer. The morphology of these deposits seems to depend on the cyto- and fibroarchitectonics of the brain region in which they are found, on the amount of amyloid deposited, and also on the type of staining technique used. It is only under specific circumstances that the deposition of amyloid in the neuropil is accompanied by the formation of paired helical filaments in nerve cell processes and their parent perikarya. In conclusion, our studies suggest that the extent of brain amyloidosis in Alzheimer's disease is much wider than so far appreciated.
The present investigation was undertaken to study the ultrastructural morphology of brain blood vessels during vasospasm following total cerebral ischemia. Global cerebral ischemia was produced in rats by compression of the cardiac vessel bundle (i.e., cardiac arrest) using a metal hook that was introduced into the mediastinum. Ischemia lasted for 10 min with blood recirculation for 6, 12 and 24 h. Rat brains were perfusion-fixed and regions from the cerebral cortex and associated leptomeningeal vessels were evaluated by scanning and transmission electron microscopy. We noted three general vasoconstrictive responses in vessels of various sizes including veins and arteries. These alterations related to the smooth muscle cell arrangement associated with each constricted vessel including a circumferential, and longitudinal arrangement, or a combination of both types. Other features in the three types of vasoconstricted vessels included thickening of the vessel basement membranes with increased endothelial microfilaments and vesicular profiles. Our studies present evidence that ischemia of 10-min duration with blood reflow for 6, 12 and 24 h produces profound and variable vasospastic changes in some but not all vessels. These vascular alterations are thought to be caused in part by vasoactive substances released both by endothelial and blood cells and by perivascular cellular elements in response to the ischemic episode.
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