Abstract
With the evidence that autopsies of demented individuals over the age of 65 demonstrate a predominance of lesions normally associated with Alzheimer’s disease, i.e., neurofibrillary tangles and “senile” (neuritic plaques) (Tomlinson et al., 1968, 1970), the significance of Alzheimer’s disease as a public health problem became evident. The correlation of plaque count with the degree of dementia further established the relationship of this pathologic lesion with clinical manifestations (Blessed et al., 1968). Another interesting and significant correlation was the pathologic evidence that Down’s syndrome individuals over the age of 40 had all the pathologic lesions of Alzheimer’s disease as well as many of the clinical manifestations (Jervis, 1948).
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Allsop, D., 1986, Biochemistry of cerebral amyloid in Alzheimer’s disease, the unconventional slow virus diseases and Icelandic cerebrovascular amyloidosis, in: Amyloidosis (J. Marrink and M. H. Van Rijswijk, eds.), Martinus Nijhoff, Dordrecht, pp. 243–253.
Allsop, D., Landon, M., Kidd, M., Lowe, J. S., Reynolds, G. P., and Gardner, A., 1986, 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. 68: 252–256.
Allsop, D., Wong, C. W., Ikeda, S., Landon, M., Kidd, M., and Glenner, G. G., 1988, Immunohistochemical evidence for the derivation of a peptide ligand from the amyloid ß-protein precursor of Alzheimer disease, Proc. Natl. Acad. Sci. USA 85: 2790–2794.
Bahmanyar, S., Higgins, G. A., Goldgaber, D., Lewis, D. A., Morrison, J. H., Wilson, M. C., Shankar, S. K., and Gajdusek, D. C., 1987, Localization of amyloid ß protein messenger RNA in brains from patients with Alzheimer’s disease, Science 237: 77–80.
Blessed, G., Tomlinson, B. E., and Roth, M., 1968, The association between quantitative measures of dementia and of senile change in the cerebral grey matter of elderly subjects, Br. J. Psychiatry 114: 797–811.
Burger, P. C., and Vogel, F. S., 1973, The development of the pathologic changes of Alzheimer’s disease and senile dementia in patients with Down’s syndrome, Am. J. Pathol. 73: 457–476.
Cohen, D. E., Feiner, H., Jensson, O., and Frangione, B., 1983, Amyloid fibril in hereditary cerebral hemorrhage with amyloidosis (HCHWA) is related to the gastroenteropancreatic neuroendocrine protein, gamma trace, J. Exp. Med. 158: 623–628.
Divry, P., and Florkin, M., 1927, Sur les propriétés optiques de l’amyloide, C. R. Soc. Biol. 97: 1808–1810.
Dwulet, F. E., and Benson, M. D., 1984, Primary structure of an amyloid prealbumin and its plasma precursor in a heredofamilial polyneuropathy of Swedish origin, Proc. Natl. Acad. Sei. USA 81: 694–698.
Eanes, E. D., and Glenner, G. G., 1968, X-ray diffraction studies of amyloid filaments, J. Histochem. Cytochem. 16: 673–677.
Epstein, C. J., 1983, Down’s syndrome and Alzheimer’s disease: Implications and approaches, in: Banbury Report 15: Biological Aspects of Alzheimer’s Disease ( R. Katzman, ed.), Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, pp. 169–182.
Fischer, O., 1910, Die presbyophrene Demenz deren anatomische Gründlage and klinische Abgrenzung, Z. Ges. Neurol. Psychiatry 3: 371–471.
Fujihara, S., Balow, J. E., Costa, J. C., and Glenner, G. G., 1980, Identification and classification of amyloid in formalin-fixed, paraffin-embedded tissue sections by the unlabeled immunoperoxidase method, Lab. Invest. 43: 358–365.
Glenner, G. G., 1979, Congophilic microangiopathy in the pathogenesis of Alzheimer’s syndrome (presenile dementia), Med. Hypoth. 5: 1231–1236.
Glenner, G. G., 1980, Amyloid deposits and amyloidosis: The ß-fibrilloses (Medical Progress Report), N. Engl. J. Med. 302: 1283–1292, 1333–1343.
Glenner, G. G., 1983, Alzheimer’s disease: Multiple cerebral amyloidosis, in: Banbury Report 15: Biological Aspects of Alzheimer’s Disease, Cold Spring Harbor Symposium ( R. Katzman, ed.), Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, pp. 137–144.
Glenner, G. G., and Wong, C. W., 1984a, Alzheimer’s disease: Initial report of the purification and characterization of a novel cerebrovascular amyloid protein, Biochem. Biophys. Res. Commun. 120: 885–890.
Glenner, G. G., and Wong, C. W., 1984b, Alzheimer’s disease and Down’s syndrome sharing of a unique cerebrovascular amyloid fibril protein, Biochem. Biophys. Res. Commun. 122: 1131–1135.
Glenner, G. G., and Wong, C., 1987, Amyloidosis in Alzheimer’s disease and Down’s syndrome, in: Banbury Report 27: Molecular Neuropathology of Aging ( P. Davies and C. E. Finch, eds.), Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, pp. 253–265.
Glenner, G. G., Ein, D., Eanes, E. D., Bladen, H. A., Terry, W., and Page, D., 1971, The creation of “amyloid” fibrils from Bence Jones proteins in vitro, Science 174: 712–714.
Glenner, G. G., Harada, M., and Isersky, C., 1972, The purification of amyloid fibril proteins, Prep. Biochem. 2: 39–51.
Glenner, G. G., Eanes, E. D., Bladen, H. A., Linke, R. P., and Termine, J. D., 1974, ß-pleated sheet fibrils: A comparison of native amyloid with synthetic protein fibrils, J. Histochem. Cytochem. 22: 1141–1158.
Glenner, G. G., Henry, J. H., and Fujihara, S., 1981, Congophilic angiopathy in the pathogenesis of Alzheimer’s degeneration, Ann. Pathol. 1: 120–129.
Glenner, G. G., Wong, C. W., Quaranta, V., and Eanes, E. D., 1984, The amyloid deposits in Alzheimer’s disease: Their nature and pathogenesis, Appl. Pathol. 83: 7908–7912.
Goldgaber, D., Lerman, M. I., McBride, O. W., Saffiotti, U., and Gadjdusek, D. C., 1987, Characterization and chromosomal localization of a cDNA encoding brain amyloid of Alzheimer’s disease, Science 23: 877–880.
Gudmundsson, G., Hallgrimasson, J., Johasson, T. A., Bjarnason, O., 1972, Hereditary cerebral hemorrhage with amyloidosis, Brain 95: 387–404.
Guiroy, D. C., Miyazaki, M., Multhaup, G., Fischer, P., Garruto, R. M., Beyreuther, K., Masters, C. L., Simms, G., Gibbs, C. J., Jr., and Gajdusek, D. C., 1987, Amyloid of neurofibrillary tangles of Guamanian parkinsonism-dementia and Alzheimer disease share identical amino acid sequence, Proc. Natl. Acad. Sci. USA 84: 2073–2077.
Heston, L. L., 1976, Alzheimer’s disease, trisomy 21, and myeloproliferative disorders: Associations suggesting a genetic diathesis, Science 196: 322–323.
Ikeda, S., Wong, C. W., Allsop, D., Landon, M., Kidd, M., and Glenner, G. G., 1987, Immunogold labeling of cerebrovascular and neuritic plaque amyloid fibrils in Alzheimer’s disease with an anti-ß-protein monoclonal antibody, Lab Invest. 57: 446–449.
Ishii, T., Haga, S., and Shimizu, F., 1975, Idnetification of components of immunoglobulins in senile plaques by means of fluorescent antibody technique, Acta Neuropathol. (Berl.) 32: 157–162.
Jenkins, E. C., Devine-Gage, E. A., Yao, X. L., Nouck, G. E., Jr., Brown, W. T., Wisniewski, H. M., and Robakis, N. K., 1987, In-situ hybridization of the beta-amyloid protein probe to chromosome 9 in patients with familial Alzheimer’s disease (Letter), Lancet 2: 1155–1156.
Jervis, G. A., 1948, Early senile dementia in mongoloid idocy, Am. J. Psychiatry 105: 102–106.
Kang, J., Lemaire, H.-G., Unterbeck, A., Salbaum, J. M., Masters, C. L., Grzeschik, K.-H., Multhaup, G., Beyreuther, K., and Müller-Hill, B., 1987, The precursor of Alzheimer’s disease amyloid A4 protein resembles a cell-surface receptor, Nature (Lond.) 325: 733–736.
Kidd, M., Allsop, D., and London, M., 1978, Senile plaque amyloid, paired helical filaments, and cerebrovascular amyloid in Alzheimer’s disease are all deposits of the same protein, (Letter), Lancet i:278.
Kirschner, D. A., Abraham, C., and Selkoe, D. J., 1986, X-ray diffraction from intraneuronal paired helical filaments and extraneuronal amyloid fibers in Alzheimer disease indicates cross-ß conformation, Proc. Natl. Acad. Sci. USA 83: 503–507.
Laemmli, U. D., 1970, Cleavage of structural proteins during the assembly of the head of bacteriophage T, Nature (Lond.) 227: 680–685.
Lovett, M., Goldgaber, D., Ashley, P., Cox, D. R., Gajdusek, D. C., and Epstein, C. J., 1987, The mouse homolog of the human amyloid ß protein (AD-AP) gene is located on the distal end of mouse chromosome 16: Further extension of the homology between human chromosome 21 and mouse chromosome 16, Biochem. Biophys. Res. Commun. 144: 1069–1075.
Marglin, A., and Merrifield, R. B., 1970, Chemical synthesis of peptides and proteins, Annu. Rev. Biochem. 39: 841–866.
Masters, C. L., Multhaup, G., Simms, G., Pottgiesser, J., Martins, R. N., and Beyreuther, K., 1985a, Neuronal origin of a cerebral amyloid: Neurofibrillary tangles of Alzheimer’s disease contain the same protein as the amyloid of plaque cores and blood vessels, EMBO J. 4: 2757–2763.
Masters, C. L., Simms, G., Weinman, N. A., Multhaup, G., McDonald, B. L., and Beyreuther, K., 1985b, Amyloid plaque core protein in Alzheimer disease and Down syndrome, Proc. Natl. Acad. Sci. USA 82: 4245–4249.
Miyakawa, T., Shimoji, A., Kuramoto, R. and Higuchi, Y., 1982, The relationship between senile plaques and cerebral blood vessels in Alzheimer’s disease and senile dementia: Morphological mechanisms of senile plaque production, Virchows Arch. [Cell Pathol.] 40: 121–129.
Pantelakis, S., 1954, Un type particulier d’angiopathie sénile du système nerveux central: l’angiopathie Congophile. Topographie et fréquence, Monatsschr. Psychiat. Neurol. 128: 219–256.
Ponte, P., Gonzalez-DeWhitt, P., Schilling, J., Miller, J., Hsu, D., Greenberg, B., Davis, K., Wallace, W., Lieberburg, I., Fuller, F., and Cordell, B., 1988, A new A4 amyloid mRNA contains a domain homologous to serine proteinase inhibitors, Nature (Lond.) 331: 525–527.
Powers, J. M., Schlaeffer, W. W., Willingham, M. C., and Hall, B. J., 1981, An immunoperoxidase study of senile plaque amyloid, J. Neuropathol. (Berl.) 39: 311 (abst.).
Prusiner, S. B., 1984, Some speculations about prions, amyloid, and Alzheimer’s disease, N. Engl. J. Med. 310: 661–663.
Robakis, N. K., Wisniewski, H. M., Jenkins, E. C., Devine-Gage, E. A., Houck, G. E., Yao, X.-L., Ramakrishna, N., Wolfe, G., Silverman, W. P., and Brown, W. T., 1987, Chromosome 21q21 sublocalisation of gene encoding beta-amyloid peptide in cerebral vessels and neuritic (senile) plaques of people with Alzheimer disease and Down syndrome (Letter), Lancet 1: 384–385.
Selkoe, D. J., Abraham, C. R., Podlisny, M. B., and Duffy, L. K., 1986, Isolation of low-molecular-weight proteins from amyloid plaque fibers in Alzheimer’s disease, J. Neurochem. 46: 1820–1834.
St. George-Hyslop, P. H., Tanzi, R. E., Polinsky, R. J., Haines, J. L., Nee, L., Watkins, P. C., Myers, R. H., Feldman, R. G., Pollen, D., Drachman, D., Growdon, J., Bruni, A., Foncin, J.-F., Salmon, D., Frommelt, P., Amaducci, L., Sorbi, S., Piacentini, S., Stewart, G. D., Hobbs, W. J., Conneally, P. M., and Gusella, J. F., 1987, The genetic defect causing familial Alzheimer’s disease maps on chromosom 21, Science 235: 885–890.
Sternberger, L. A., 1979, Immunocytochemistry, 2nd ed., Wiley, New York, 104–169.
Surbeck, E. B., 1961, L’angiopathie dyshorique (Morel) de l’écorce cérébrale: étude anatomoclinique el statistique: aspect génétique, Acta Neuropathol. (Berl.) 1: 168–197.
Tanzi, R. E., Gusella, J. F., Watkins, P. C., Bruns, G. A. P., St.-George-Hyslop, P., VanKeuren, M. L., Patterson, D., Pagan, S., Kurnit, D. M., and Neve, R. L., 1987, Amyloid p protein gene: cDNA, mRNA distribution, and genetic linkage near the Alzheimer locus, Science 235: 880–884.
Tanzi, R. E., McClatchey, A. I., Lamperti, E. D., Villa-Komaroff, L., Gusella, J. F., and Neve, R. L., 1988, Protease inhibitor domain encoded by an amyloid protein precursor mRNA associated with Alzheimer’s disease, Nature (Lond.) 331: 528–532.
Tomlinson, B. E., Blessed, G., and Roth, M., 1968, Observations on the brains of non-demented old people, J. Neurol. Sci. 7: 331–356.
Tomlinson, B. E., Blessed, G., and Roth, M., 1970, Observations on the brains of demented old people, J. Neurol Sci. 11: 205–242.
Torack, R. M., 1975, Congophilic angiopathy complicated by surgery and massive hemorrhage, Am. J. Pathol. 81: 349–366.
Van Broeckhoven, C., Genthe, A. M., Vandenberghe, A., Horsthemke, B., Backhovens, H., Raeymaekers, P., Van Hul, W., Wehnert, A., Gheuens, J., Cras, P., Bruyland, M., Martin, J. J., Salbaum, M., Multhaup, G., Masters, C. L., Beyreuther, K., Gurling, H. M. D., Mullan, M. J., Holland, A., Barton, A., Irving, N., Williamson, R., Richards, S. J., and Hardy, J. A., 1987, Failure of familial Alzheimer’s disease to segregate with the A4-amyloid gene in several European families, Nature (Lond.) 329: 153–155.
van Duinen, S. G., Castano, E. M., Prelli, F., Bots, G. T. A. B., Luyendijk, W., and Frangione, B., 1987, Hereditary cerebral hemorrhage with amyloidosis in patients of Dutch origin is related to Alzheimer disease, Proc. Natl. Acad. Sci. USA 84: 5991–5994.
Walter, G., and Doolittle, R. R., 1983, Antibodies against synthetic peptides, in: Genetic Engineering: Principles and Methods, Vol. 5 ( J. K. Setlow, and A. Hollaender, eds.), Plenum, New York, pp. 61–91.
Wong, C. W., Quaranta, W. V., and Glenner, G. G., 1985, Neuritic plaques and cerebrovascular amyloid in Alzheimer disease are antigenically related, Proc. Natl. Acad. Sci. USA 82: 8729–8732.
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© 1990 Plenum Press, New York
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Glenner, G.G. (1990). Alzheimer’s Disease. In: Goldstein, A.L. (eds) Biomedical Advances in Aging. GWUMC Department of Biochemistry Annual Spring Symposia. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0513-2_5
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DOI: https://doi.org/10.1007/978-1-4613-0513-2_5
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