CONSERVATION OF BRAIN AMYLOID PROTEINS IN AGED MAMMALS AND HUMANS WITH ALZHEIMERS-DISEASE

被引:425
作者
SELKOE, DJ
BELL, DS
PODLISNY, MB
PRICE, DL
CORK, LC
机构
[1] BRIGHAM & WOMENS HOSP, CTR NEUROL DIS, DEPT MED NEUROL, BOSTON, MA 02115 USA
[2] JOHNS HOPKINS UNIV, SCH MED, DEPT PATHOL, DIV COMPARAT MED, BALTIMORE, MD 21205 USA
[3] JOHNS HOPKINS UNIV, SCH MED, DEPT PATHOL, NEUROPATHOL LAB, BALTIMORE, MD 21205 USA
[4] JOHNS HOPKINS UNIV, SCH MED, DEPT NEUROL, BALTIMORE, MD 21205 USA
[5] JOHNS HOPKINS UNIV, SCH MED, DEPT NEUROSCI, BALTIMORE, MD 21205 USA
关键词
D O I
10.1126/science.3544219
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:873 / 877
页数:5
相关论文
共 28 条
  • [1] MONOCLONAL-ANTIBODIES SHOW THAT NEUROFIBRILLARY TANGLES AND NEUROFILAMENTS SHARE ANTIGENIC DETERMINANTS
    ANDERTON, BH
    BREINBURG, D
    DOWNES, MJ
    GREEN, PJ
    TOMLINSON, BE
    ULRICH, J
    WOOD, JN
    KAHN, J
    [J]. NATURE, 1982, 298 (5869) : 84 - 86
  • [2] ALZHEIMERS-DISEASE - INITIAL REPORT OF THE PURIFICATION AND CHARACTERIZATION OF A NOVEL CEREBROVASCULAR AMYLOID PROTEIN
    GLENNER, GG
    WONG, CW
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1984, 120 (03) : 885 - 890
  • [3] GLENNER GG, 1981, ANN PATHOL, V1, P120
  • [4] GLENNER GG, 1983, BIOL ASPECTS ALZHEIM, P127
  • [5] ABNORMAL PHOSPHORYLATION OF THE MICROTUBULE-ASSOCIATED PROTEIN-TAU (TAU) IN ALZHEIMER CYTOSKELETAL PATHOLOGY
    GRUNDKEIQBAL, I
    IQBAL, K
    TUNG, YC
    QUINLAN, M
    WISNIEWSKI, HM
    BINDER, LI
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1986, 83 (13) : 4913 - 4917
  • [6] GRUNDKEIQBAL I, 1986, J BIOL CHEM, V261, P6084
  • [7] ANTIBODIES TO PAIRED HELICAL FILAMENTS IN ALZHEIMERS-DISEASE DO NOT RECOGNIZE NORMAL BRAIN PROTEINS
    IHARA, Y
    ABRAHAM, C
    SELKOE, DJ
    [J]. NATURE, 1983, 304 (5928) : 727 - 730
  • [8] PHOSPHORYLATED TAU PROTEIN IS INTEGRATED INTO PAIRED HELICAL FILAMENTS IN ALZHEIMERS-DISEASE
    IHARA, Y
    NUKINA, N
    MIURA, R
    OGAWARA, M
    [J]. JOURNAL OF BIOCHEMISTRY, 1986, 99 (06) : 1807 - 1810
  • [9] JOACHIM CL, 1986, NEUROLOGY, V36, P226
  • [10] EVIDENCE FOR CHOLINERGIC NEURITES IN SENILE PLAQUES
    KITT, CA
    PRICE, DL
    STRUBLE, RG
    CORK, LC
    WAINER, BH
    BECHER, MW
    MOBLEY, WC
    [J]. SCIENCE, 1984, 226 (4681) : 1443 - 1445