Hostname: page-component-78c5997874-g7gxr Total loading time: 0 Render date: 2024-11-13T01:39:00.638Z Has data issue: false hasContentIssue false
  • English
  • Français

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  and
M.J. Ball
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
Rights & Permissions [Opens in a new window]

Abstract:

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

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
Information
Canadian Journal of Neurological Sciences , Volume 13 , Issue S4 , November 1986 , pp. 456 - 461
Copyright
Copyright © Canadian Neurological Sciences Federation 1986

References

1.Tomlinson, BE, Corsellis, JAN. Ageing and the dementias. In: Adams, JH, Corsellis, JAN, Duchen, LW, eds. Greenfield’s Neuropathology, 4th ed. New York: John Wiley and Sons. 1984: 951–1025.Google Scholar
2.Morimatsu, M, Hirai, S, Muramatsu, A, et al. Senile degenerative brain lesions and dementia. J Am Geriatr Soc 1975; 23: 390–406.CrossRefGoogle ScholarPubMed
3.Mancardi, GL, Perdelli, F, Rivano, C, et al. Thickening of the basement membrane of cortical capillaries in Alzheimer’s disease. Acta Neuropathol (Berl) 1980; 49: 79–83.CrossRefGoogle ScholarPubMed
4.Bell, MA, Ball, MJ. Morphometric comparison of hippocampal microvasculature in ageing and demented people: diameters and densities. Acta Neuropathol (Berl) 1981; 53: 299–318.CrossRefGoogle ScholarPubMed
5.Ball, MJ. Neuronal loss, neurofibrillary tangles, and granulovacuolar degeneration in the hippocampus with ageing and dementia. Acta Neuropathol (Berl) 1977; 37: 111–118.CrossRefGoogle ScholarPubMed
6.Ball, MJ. Histotopography of cellular changes in Alzheimer’s disease. In: Nandy, K, ed. Senile dementia: a biomedical approach. New York: Elsevier, 1978: 89–104.Google Scholar
7.Tomlinson, BE, Henderson, G.Some quantitative cerebral findings in normal and demented old people. In: Terry, RD, Gershon, S, eds. Neurobiology of Aging. New York: Raven Press, 1976: 183–204.Google Scholar
8.Bell, MA, Ball, MJ. Laminar variation in the microvascular architecture of normal human visual cortex (area 17). Br Res 1985; 335: 139–143.CrossRefGoogle ScholarPubMed
9.Mandybur, Tl. The incidence of cerebral amyloid angiopathy in Alzheimer’s disease. Neurol 1975; 25: 120–126.CrossRefGoogle ScholarPubMed
10.Bell, MA, Scarrow, WG. Staining for microvascular alkaline phosphatase in thick celloidin sections of nervous tissue: morphometric and pathological applications. Microvasc Res 1984; 27: 189–203.CrossRefGoogle ScholarPubMed