Neuritic plaques and vessels of visual cortex in aging and Alzheimer's dementia

Changes in microvascular dimensions occurring with normal aging and Alzheimer's dementia were measured in thick sections of postmortem human visual cortex stained for alkaline phosphatase. Capillary density was decreased to the same degree in both normal aged and demented aged subjects. The fie...

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Published inNeurobiology of aging Vol. 11; no. 4; pp. 359 - 370
Main Authors Bell, Mary A., Ball, Melvyn J.
Format Journal Article
LanguageEnglish
Published London Elsevier Inc 01.07.1990
Elsevier Science
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ISSN0197-4580
1558-1497
DOI10.1016/0197-4580(90)90001-G

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Summary:Changes in microvascular dimensions occurring with normal aging and Alzheimer's dementia were measured in thick sections of postmortem human visual cortex stained for alkaline phosphatase. Capillary density was decreased to the same degree in both normal aged and demented aged subjects. The fields selected for analysis in both groups included all cortical laminae and, where possible, amyloid-cored neuritic plaques. The mean density of such plaques in these selected fields was slightly but not significantly higher in the demented group. In both groups plaques were more plentiful in visual laminae with the highest capillary densities (II–IV), but plaques and vessels were closer to each other in the normal aged than in the demented. Plaque distributions differed; in the normal aged, plaques concentrated in lamina IV; in the demented they were more evenly spread throughout the laminae. Plaque cores were larger in the demented. Amyloid angiopathy was more common and more extensive in the demented group; amyloid-cored plaques were not closely associated with affected vessels. Plaque distributions in Alzheimer subjects with and without amyloid angiopathy differed; plaque density was greatest in those without angiopathy. Alzheimer's dementia was not associated with any decline in microvascularity. Plaque concentration in well vascularized laminae suggests a pathogenetic role for some blood-borne agent. Differences in plaque distributions imply that the role or the agent differs in normal and demented aging, or perhaps between cases with and without amyloid angiopathy.
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ISSN:0197-4580
1558-1497
DOI:10.1016/0197-4580(90)90001-G