Hostname: page-component-77c89778f8-gq7q9 Total loading time: 0 Render date: 2024-07-16T21:58:18.307Z Has data issue: false hasContentIssue false
  • English
  • Français

Amyloid Angiopathy in Alzheimer's Disease

Published online by Cambridge University Press:  18 September 2015

C. Bergeron ,
P.J. Ranalli  and
P.N. Miceli
C. Bergeron*
Affiliation:
Department of Pathology (Neuropathology), Faculty of Medicine, University of Toronto
P.J. Ranalli
Affiliation:
Department of Medicine (Neurology), Faculty of Medicine, University of Toronto
P.N. Miceli
Affiliation:
Department of Biostatistics, Ontario Cancer Institute, Toronto
*
Department of Pathology, Toronto General Hospital, EC-4-316, 200 Elizabeth Street, Toronto, Ontario, Canada M5G 2C4
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.

Thirty cases of Alzheimer's disease and 30 age-matched controls were studied to determine the incidence of cerebral amyloid angiopathy and its relationship to age, neuritic plaque formation, and amyloid plaque content. Cerebral amyloid angiopathy (CAA) was present in 86% of AD cases and 40% of age-matched controls. Its frequent occurrence in AD is not merely a reflection of the advancing age of this group: it was seen only in the presence of neuritic plaques, regardless of age, and represents an integral component of AD. Neuritic plaques however, did occur in the absence of CAA in 17% of all cases. The amount of vascular and plaque amyloid tended to be of comparable severity in many cases, but significant discrepancies were observed, with preferential deposition of amyloid in either plaque or vessel. Our results suggest that neuritic plaque formation and amyloid deposition are linked genetically or etiologically, but independently expressed, without a cause-and-effect relationship.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 14 , Issue 4 , November 1987 , pp. 564 - 569
Copyright
Copyright © Canadian Neurological Sciences Federation 1987

References

1.Glenner, GG, Henry, JH, Shigeyoshi, F. Congophilic angiopathy in the pathogenesis of Alzheimer’s degeneration. Ann Pathol 1981; 1: 120–129.Google ScholarPubMed
2.Glenner, GG. Alzheimer’s Disease. Multiple cerebral amyloidosis. In: Katzman, R, ed. Banbury Report 15, Biological Aspects of Alzheimer’s Disease. Cold Spring Harbor Laboratory, 1983; 137–143.Google Scholar
3.Mandybur, TI. The incidence of cerebral amyloid angiopathy in Alzheimer’s disease. Neurology 1975; 25: 120–126.CrossRefGoogle ScholarPubMed
4.Esiri, MM, Wilcock, GK. Cerebral amyloid angiopathy in dementia and old age. J Neurol Neurosurg Psychiatry 1986; 49: 1221–1226.CrossRefGoogle ScholarPubMed
5.Tomonaga, M. Cerebral amyloid angiopathy in the elderly. J Am Geriatr Soc 1981; 29: 151–157.CrossRefGoogle ScholarPubMed
6.Vinters, HV, Gilbert, JJ. Cerebral amyloid angiopathy: Incidence and complications in the ageing brain. II. The distribution of amyloid vascular changes. Stroke 1983; 14: 924–928.CrossRefGoogle ScholarPubMed
7.Pantelakis, S. Un type particulier d’angiopathie senile du système nerveux central: l’angiopathie congophile: topographie et fréquence. Monatsschr Psychiat Neurol 1954; 128: 219–256.CrossRefGoogle Scholar
8.Surbek, B. L’angiopathie dyshorique(Morel)de l’ecorcecerebrale. Etude anatomo-clinique et statistique, aspect génétique. Acta Neuropathol (Beri) 1961; 1: 168–197.CrossRefGoogle Scholar
9.Brown, MB. BMDP Statistical Software, 1983 Printing with additions, Chapter 11. University of California Press.Google Scholar
10.Cohen, J. Some statistical issues in psychological research. In: Wolman, B, ed. Handbook of Clinical Psychology. New York, McGraw Hill, 1965.Google Scholar
11.Cochran, WG. Some methods for strengthening the common chisquare test. Biometrics 1954; 10: 4170–441.CrossRefGoogle Scholar
12.SAS Institute Inc. SAS/GRAPH User’s guide. Version 5 edition. Gary, N.C. U.S.A., 1985.Google Scholar
13.Mountjoy, CQ, Tomlinson, BE, Gibson, PH. Amyloid and senile plaques and cerebral blood vessels. A semi-quantitative investigation of the possible relationship. J Neurol Sci 1982; 57: 89–103.CrossRefGoogle ScholarPubMed
14.Pro, JD, Smith, CH, Sumi, SM. Presenile Alzheimer’s Disease: Amyloid plaques in the cerebellum. Neurology 1980; 30: 820–825.CrossRefGoogle ScholarPubMed
15.Rudelli, RD, Wisniewski, HM. Cerebellar amyloid plaques in Alzheimer’s dementia (AD) and senile dementia of Alzheimer type (SDAT). J Neuropathol Exp Neurol 1985; 44: 364.CrossRefGoogle Scholar
16.Mandybur, TI. Cerebral amyloid angiopathy: The vascular pathology and complications. J Neuropathol Exp Neurol 1986; 45: 79–90.CrossRefGoogle ScholarPubMed
17.Schwartz, P. Amyloidosis of the nervous system in the aged. In: Minkler, J, ed. Pathology of the Nervous System, New York. McGraw-Hill, 1972, volume 3: 2812–2848.Google Scholar
18.Wong, C W, Quaranta, V, Glenner, GG. Neuritic plaques and cerebrovascular amyloid in Alzheimer’s Disease are antigenetically related. Proc Natl Acad Sci USA 1985; 82: 8729–8732.CrossRefGoogle Scholar
19.Masters, CL, Multhaup, G, Simms, G, et al. Neuronal origin of a cerebral amyloid. Neurofibrillary tangles of Alzheimer’s disease contain the same protein as the amyloid of plaques and blood vessels. Embo J 1985; 4: 2757–2763.CrossRefGoogle ScholarPubMed
20.Tanzi, RE, Gusella, JF, Watkins, PC, et al. Amyloid B protein gene: cDN A, mRNA distribution, and genetic linkage near the Alzheimer locus. Science 1987; 235: 880–884.CrossRefGoogle Scholar
21.Goldgaber, D, Lerman, MI, McBride, OW. Characterization and chromosomal localization of a cDNA encoding brain amyloid of Alzheimer’s disease. Science 1987; 235: 877–880.CrossRefGoogle ScholarPubMed
22.Miyakawa, T, Shimoji, A, Kuramoto, R, et al. The relationship between senile plaques and cerebral blood vessels in Alzheimer’s disease and senile dementia. Virchows Arch (Cell Pathol) 1981; 40: 121–129.CrossRefGoogle Scholar
23.Kidd, M. Alzheimer’s disease. An electron microscopical study. Brain 1964; 87: 307–320.CrossRefGoogle ScholarPubMed
24.Wisniewski, HM, Terry, RD. Re-examination of the pathogenesis of the senile plaque. In: Zimmerman, HM, ed. Progress in Neuropathology, New York, Grune and Stratton, 1972, vol. 2: 1–26.Google Scholar
25.Friede, RL, Magee, KR. Alzheimer’s disease. Presentation of a case with pathologic and enzymatic-histochemical observations. Neurology 1962; 12: 213–222.CrossRefGoogle Scholar
26.Pearson, RCA, Esiri, MM, Hiorns, RW, et al. Anatomical correlates of the distribution of the pathological changes in the neocortex in Alzheimer’s disease. Proc Natl Acad Sci USA 1985; 82: 4531–34.CrossRefGoogle Scholar
27.Duyckaerts, C, Hauw, JJ, Bastenaire, F, et al. Laminar distribution of neocortical senile plaques in senile dementia of the Alzheimer type. Acta Neuropathol 1986; 70: 249–256.CrossRefGoogle ScholarPubMed
28.Kidd, M, Allsop, D, Landon, M. Senile plaque amyloid, paired helical filaments, and cerebrovascular amyloid in Alzheimer’s disease are all deposits of the same protein. Lancet 1985; 1: 278.CrossRefGoogle ScholarPubMed
29.Allsop, D, Landon, M, Kidd, M, et al. Monoclonal antibodies raised against a subsequence of senile plaque core protein react with plaque cores, plaque periphery and cerebrovascular amyloid in Alzheimer’s disease. Neurosci Lett 1986; 68: 252–256.CrossRefGoogle ScholarPubMed
30.Selkoe, DJ, Abraham, CR, Podlisny, MB, et al. Isolation of low molecular weight proteins from amyloid plaque fibers in Alzheimer’s disease. J Neurochem 1986; 46: 1820–1834.CrossRefGoogle ScholarPubMed
31.MacDonald, SM, Esiri, MM. Monoclonal antibody binding to congophilic elements in human Alzheimer brain. J Clin Pathol 1986; 39: 1199–1203.CrossRefGoogle ScholarPubMed