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The Correlation of Vascular Capacity with the Parenchymal Lesions of Alzheimer's Disease

Published online by Cambridge University Press:  18 September 2015

M.A. Bell*
Affiliation:
Departments of Pathology and Clinical Neurological Sciences, University of Western Ontario, London, Ontario
M.J. Ball
Affiliation:
Departments of Pathology and Clinical Neurological Sciences, University of Western Ontario, London, Ontario
*
Department of Radiology, Bowman Gray School of Medicine, 300 S. Hawthorne Road, Winston-Salem, N.C. U.S.A. 27103
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Abstract:

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Hippocampal capillary and arteriolar measurements showed a significant reduction in capacity with normal aging. Alzheimer's dementia was not associated with any further reduction; in fact regional variations suggested that the zones of Amnion's horn most severely affected by tangles and granulovacuoles retained the best vascular capacity.

The arterial system supplying the hippocampus, from the posterior cerebral artery to the series of small hippocampal arteries, was also assessed. Its capacity, as judged by arterial diameters, was similarly found to decrease significantly with age; the arterial diameters of Alzheimer cases were (insignificantly) greater than those of the normal old.

Calcarine capillary and arteriolar measurements also indicated a marked reduction of capacity with normal aging, and, as before, in Alzheimer's dementia there was no further significant change. All three phases of the study thus suggest that cerebrovascular capacity in Alzheimer's dementia is at least as good as in the normal old, if not better.

Senile (neuritic) plaques with amyloid cores and their relationship to the microvasculature were examined in the calcarine cortex. In both normal old and Alzheimer cases the plaques tended to congregate where capillaries were densest. Their correlation with capillary density was however better in the normal old, raising the question of whether their pathogenesis might differ in the two conditions.

Type
Cellular Clues to Pathogenesis
Copyright
Copyright © Canadian Neurological Sciences Federation 1986

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