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Cited by 377

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Conservation of brain amyloid proteins in aged mammals and humans with Alzheimer's disease.

Selkoe, Dennis J., Bell, Douglas S., Podlisny, Marcia B., Price, Donald L., Cork, Linda C.·1987·Science
DOI 10.1126/science.3544219
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Abstract

The formation of clusters of altered axons and dendrites surrounding extracellular deposits of amyloid filaments (neuritic plaques) is a major feature of the human brain in both aging and Alzheimer's disease. A panel of antibodies against amyloid filaments and their constituent proteins from humans with Alzheimer's disease cross-reacted with neuritic plaque and cerebrovascular amyloid deposits in five other species of aged mammals, including monkey, orangutan, polar bear, and dog. Antibodies to a 28-amino acid peptide representing the partial protein sequence of the human amyloid filaments recognized the cortical and microvascular amyloid of all of the aged mammals examined. Plaque amyloid, plaque neurites, and neuronal cell bodies in the aged animals showed no reaction with antibodies to human paired helical filaments. Thus, with age, the amyloid proteins associated with progressive cortical degeneration in Alzheimer's disease are also deposited in the brains of other mammals. Aged primates can provide biochemically relevant models for principal features of Alzheimer's disease: cerebrovascular amyloidosis and neuritic plaque formation.

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Crossref · 10.1126/science.3544219

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1 of 1 references verified0 citation errors · 0 not checkable

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  • In human mutant APP mouse models, a close relationship is seen between high plasma cholesterol and brain vessel amyloidosis.

    “Interestingly, the present transgenic mice showed early cerebrovascular β-amyloidosis that was exacerbated with age, in the same way that, in human mutant APP mouse models, a close relationship is seen between high plasma cholesterol and brain vessel amyloidosis [49], [50].”

    From ApoB100/LDLR-/- Hypercholesterolaemic Mice as a Model for Mild Cognitive Impairment and Neuronal Damage (2011) · cites this paper as [50]

  • Many of the mouse models for genetic AD that harbour different human APP mutations have also been shown to exhibit CAA.

    “Indeed, many of the mouse models for genetic AD that harbour different human APP mutations have also been shown to exhibit CAA [49], [50], although the overexpression of APP alone causes no Aβ deposition in most mouse lines [51], and mouse app does not generate amyloid plaques.”

    From ApoB100/LDLR-/- Hypercholesterolaemic Mice as a Model for Mild Cognitive Impairment and Neuronal Damage (2011) · cites this paper as [50]

Citations

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Research works printed but not linked: 27

  1. ANDERTON, B.H., MONOCLONAL-ANTIBODIES SHOW THAT NEUROFIBRILLARY TANGLES AND NEUROFILAMENTS SHARE ANTIGENIC DETERMINANTS, NATURE 298: 84 (1982). · DOI
  2. GLENNER, G.G., CONGOPHILIC ANGIOPATHY IN THE PATHOGENESIS OF ALZHEIMERS DEGENERATION, ANNALES DE PATHOLOGIE 1: 120 (1981).
  3. 10.1016/S0006-291X(84)80190-4 · DOI · Paper page
  4. GLENNER, G.G., BIOL ASPECTS ALZHEIM: 127 (1983).
  5. GRUNDKEIQBAL, I, MICROTUBULE-ASSOCIATED PROTEIN-TAU - A COMPONENT OF ALZHEIMER PAIRED HELICAL FILAMENTS, JOURNAL OF BIOLOGICAL CHEMISTRY 261: 6084 (1986). · DOI
  6. GRUNDKEIQBAL, I, ABNORMAL PHOSPHORYLATION OF THE MICROTUBULE-ASSOCIATED PROTEIN-TAU (TAU) IN ALZHEIMER CYTOSKELETAL PATHOLOGY, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 83: 4913 (1986).
  7. IHARA, Y, PHOSPHORYLATED TAU PROTEIN IS INTEGRATED INTO PAIRED HELICAL FILAMENTS IN ALZHEIMERS-DISEASE, JOURNAL OF BIOCHEMISTRY 99: 1807 (1986).
  8. IHARA, Y, ANTIBODIES TO PAIRED HELICAL FILAMENTS IN ALZHEIMERS-DISEASE DO NOT RECOGNIZE NORMAL BRAIN PROTEINS, NATURE 304: 727 (1983). · DOI
  9. JOACHIM, C.L., AUTOPSY NEUROPATHOLOGY IN 76 CASES OF CLINICALLY DIAGNOSED ALZHEIMERS-DISEASE, NEUROLOGY 36: 226 (1986).
  10. KITT, C.A., CATECHOLAMINERGIC NEURITES IN SENILE PLAQUES IN PREFRONTAL CORTEX OF AGED NONHUMAN-PRIMATES, NEUROSCIENCE 16: 691 (1985). · DOI
  11. 10.1126/science.6505701 · DOI
  12. KOSIK, K.S., MICROTUBULE-ASSOCIATED PROTEIN TAU (TAU) IS A MAJOR ANTIGENIC COMPONENT OF PAIRED HELICAL FILAMENTS IN ALZHEIMER-DISEASE, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 83: 4044 (1986).
  13. MASTERS, C.L., NEURONAL ORIGIN OF A CEREBRAL AMYLOID - NEUROFIBRILLARY TANGLES OF ALZHEIMERS-DISEASE CONTAIN THE SAME PROTEIN AS THE AMYLOID OF PLAQUE CORES AND BLOOD-VESSELS, EMBO JOURNAL 4: 2757 (1985). · DOI
  14. 10.1073/pnas.82.12.4245 · DOI · Paper page
  15. MIYAKAWA, T, THE RELATIONSHIP BETWEEN SENILE PLAQUES AND CEREBRAL BLOOD-VESSELS IN ALZHEIMERS-DISEASE AND SENILE DEMENTIA - MORPHOLOGICAL MECHANISM OF SENILE PLAQUE PRODUCTION, VIRCHOWS ARCHIV B-CELL PATHOLOGY INCLUDING MOLECULAR PATHOLOGY 40: 121 (1982). · DOI
  16. NUKINA, N, ONE OF THE ANTIGENIC DETERMINANTS OF PAIRED HELICAL FILAMENTS IS RELATED TO TAU PROTEIN, JOURNAL OF BIOCHEMISTRY 99: 1541 (1986). · DOI
  17. SELKOE, D.J., ISOLATION OF LOW-MOLECULAR-WEIGHT PROTEINS FROM AMYLOID PLAQUE FIBERS IN ALZHEIMERS-DISEASE, JOURNAL OF NEUROCHEMISTRY 46: 1820 (1986). · DOI
  18. STRUBLE, R.G., SOMATOSTATINERGIC NEURITES IN SENILE PLAQUES OF AGED NON-HUMAN PRIMATES, BRAIN RESEARCH 324: 394 (1984). · DOI
  19. STRUBLE, R.G., SENILE PLAQUES IN CORTEX OF AGED NORMAL MONKEYS, BRAIN RESEARCH 361: 267 (1985). · DOI
  20. 10.1126/science.6803359 · DOI
  21. TOMLINSON, B.E., GREENFIELDS NEUROPAT: 951 (1984).
  22. TOMLINSON, B.E., OBSERVATIONS ON BRAINS OF NON-DEMENTED OLD PEOPLE, JOURNAL OF THE NEUROLOGICAL SCIENCES 7: 331 (1968). · DOI · Paper page
  23. VANLEY, C.T., CEREBRAL AMYLOID ANGIOPATHY, HUMAN PATHOLOGY 12: 609 (1981). · DOI
  24. WALKER, L.C., GLUTAMIC-ACID DECARBOXYLASE-LIKE IMMUNOREACTIVE NEURITES IN SENILE PLAQUES, NEUROSCIENCE LETTERS 59: 165 (1985). · DOI
  25. WISNIEWSKI, H, SENILE PLAQUES AND CEREBRAL AMYLOIDOSIS IN AGED DOGS - A HISTOCHEMICAL AND ULTRASTRUCTURAL STUDY, LABORATORY INVESTIGATION 23: 287 (1970).
  26. WONG, C.W., NEURITIC PLAQUES AND CEREBROVASCULAR AMYLOID IN ALZHEIMER-DISEASE ARE ANTIGENICALLY RELATED, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 82: 8729 (1985).
  27. WOOD, J.G., NEUROFIBRILLARY TANGLES OF ALZHEIMER-DISEASE SHARE ANTIGENIC DETERMINANTS WITH THE AXONAL MICROTUBULE-ASSOCIATED PROTEIN TAU (TAU), PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 83: 4040 (1986).

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Metadata

Authors
Selkoe, D. J., Bell, D. S., Podlisny, M. B., Price, D. L., & Cork, L. C.
Affiliations
  • Department of Neurology (Neuroscience), Harvard Medical School, and Center for Neurologic Diseases, Department of Medicine (Neurology), Brigham and Women's Hospital, Boston, MA 02115
  • Division of Comparative Medicine and Neuropathology Laboratory, Departments of Pathology, Neurology and Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Venue
Science
Publisher
American Association for the Advancement of Science (AAAS)
Published
1987-02-20
Volume
235
Issue
4791
Pages
873-877
ISSN
  • 0036-8075
  • 1095-9203
DOI
10.1126/science.3544219
Cited by
377
References
1
Language
en

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