Amyloid β protein 1-40 and 1-42 levels in matched cerebrospinal fluid and plasma from patients with Alzheimer disease

被引:204
作者
Mehta, PD
Pirttila, T
Patrick, BA
Barshatzky, M
Mehta, SP
机构
[1] New York State Inst Basic Res Dev Disabil, Dept Immunol, Staten Isl, NY 10314 USA
[2] Kuopio Univ Hosp, Dept Neurol, SF-70210 Kuopio, Finland
关键词
Alzheimer disease; amyloid beta protein; alpha; 1-antichymotrypsin; apolipoprotein E; enzyme linked immunosorbent assay;
D O I
10.1016/S0304-3940(01)01754-2
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We quantitated amyloid beta proteins 1-40 (A beta 40) and 1-42 (A beta 42), and alpha1-antichymotrypsin (ACT) in matched cerebrospinal fluid (CSF) and plasma of 50 patients with probable Alzheimer disease, and analyzed the relationships with age, sex, Mini-Mental State Examination (MMSE), and apolipoprotein E phenotype. There was no relation between CSF A beta 40 and A beta 42 levels with those of plasma. CSF and plasma A beta 40 and A beta 42 levels showed no association with age, sex, and MMSE score. There was a significant correlation between CSF ACT and plasma ACT levels. The data suggest that plasma ACT crosses the blood-brain barrier. However, a lack of correlation between CSF A beta 40 and A beta 42 levels with those of plasma suggests that A beta in CSF and plasma originates from different sources. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:102 / 106
页数:5
相关论文
共 21 条
  • [1] IMMUNOCHEMICAL IDENTIFICATION OF THE SERINE PROTEASE INHIBITOR ALPHA-1-ANTICHYMOTRYPSIN IN THE BRAIN AMYLOID DEPOSITS OF ALZHEIMERS-DISEASE
    ABRAHAM, CR
    SELKOE, DJ
    POTTER, H
    [J]. CELL, 1988, 52 (04) : 487 - 501
  • [2] Neuronal overexpression of mutant amyloid precursor protein results in prominent deposition of cerebrovascular amyloid
    Calhoun, ME
    Burgermeister, P
    Phinney, AL
    Stalder, M
    Tolnay, M
    Wiederhold, KH
    Abramowski, D
    Sturchler-Pierrat, C
    Sommer, B
    Staufenbiel, M
    Jucker, M
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (24) : 14088 - 14093
  • [3] PLATELETS ARE THE PRIMARY SOURCE OF AMYLOID BETA-PEPTIDE IN HUMAN BLOOD
    CHEN, M
    INESTROSA, NC
    ROSS, GS
    FERNANDEZ, HL
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1995, 213 (01) : 96 - 103
  • [4] High cerebrospinal fluid tau and low amyloid β42 levels in the clinical diagnosis of Alzheimer disease and relation to apolipoprotein E genotype
    Galasko, D
    Chang, L
    Motter, R
    Clark, CM
    Kaye, J
    Knopman, D
    Thomas, R
    Kholodenko, D
    Schenk, D
    Lieberburg, I
    Miller, B
    Green, R
    Basherad, R
    Kertiles, L
    Boss, MA
    Seubert, P
    [J]. ARCHIVES OF NEUROLOGY, 1998, 55 (07) : 937 - 945
  • [5] GhersiEgea JF, 1996, J NEUROCHEM, V67, P880
  • [6] AMYLOID-BETA PROTEIN (A-BETA) IN ALZHEIMERS-DISEASE BRAIN - BIOCHEMICAL AND IMMUNOCYTOCHEMICAL ANALYSIS WITH ANTIBODIES SPECIFIC FOR FORMS ENDING AT A-BETA-40 OR A-BETA-42(43)
    GRAVINA, SA
    HO, LB
    ECKMAN, CB
    LONG, KE
    OTVOS, L
    YOUNKIN, LH
    SUZUKI, N
    YOUNKIN, SG
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (13) : 7013 - 7016
  • [7] KATAOKA S, 1994, CLIN CHEM, V40, P11
  • [8] PASSAGE OF HUMAN AMYLOID BETA-PROTEIN-1-40 ACROSS THE MURINE BLOOD-BRAIN-BARRIER
    MANESS, LM
    BANKS, WA
    PODLISNY, MB
    SELKOE, DJ
    KASTIN, AJ
    [J]. LIFE SCIENCES, 1994, 55 (21) : 1643 - 1650
  • [9] ALPHA-1-ANTICHYMOTRYPSIN AS A POSSIBLE BIOCHEMICAL MARKER FOR ALZHEIMER-TYPE DEMENTIA
    MATSUBARA, E
    HIRAI, S
    AMARI, M
    SHOJI, M
    YAMAGUCHI, H
    OKAMOTO, K
    ISHIGURO, K
    HARIGAYA, Y
    WAKABAYASHI, K
    [J]. ANNALS OF NEUROLOGY, 1990, 28 (04) : 561 - 567
  • [10] Mayeux R, 1999, ANN NEUROL, V46, P412, DOI 10.1002/1531-8249(199909)46:3<412::AID-ANA19>3.0.CO