Different CSF β-amyloid processing in Alzheimer's and Creutzfeldt-Jakob disease

被引:14
|
作者
Mollenhauer, Brit [1 ,2 ]
Esselmann, Hermann [3 ]
Roeber, Sigrun [4 ]
Schulz-Schaeffer, Walter J. [5 ]
Trenkwalder, Claudia [1 ,2 ]
Bibl, Mirko [6 ]
Steinacker, Petra [7 ]
Kretzschmar, Hans A. [4 ]
Wiltfang, Jens [3 ]
Otto, Markus [7 ]
机构
[1] Paracelsus Elena Klin, Kassel, Germany
[2] Univ Gottingen, Gottingen, Germany
[3] Univ Duisburg Essen, Dept Psychiat, Rhein Kliniken Essen, D-45136 Essen, Germany
[4] Univ Munich, Dept Neuropathol, Munich, Germany
[5] Univ Med Ctr, Dept Neuropathol, Gottingen, Germany
[6] Univ Duisburg Essen, Kliniken Essen Mitte, Dept Psychiat Psychotherapy & Addict Med, D-45136 Essen, Germany
[7] Univ Ulm, Dept Neurol, D-7900 Ulm, Germany
关键词
beta-amyloid; beta-amyloid plaques Creutzfeldt-Jakob disease; Alzheimer's disease; Cerebrospinal fluid; CEREBROSPINAL-FLUID; PRECURSOR PROTEIN; PRION PROTEIN; PEPTIDES; GENERATION; PATTERNS;
D O I
10.1007/s00702-010-0543-z
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Decreased levels of beta-amyloid (A beta) 1-42 in cerebrospinal fluid (CSF) are characteristic for Alzheimer's disease (AD) and are also evident in Creutzfeldt-Jakob disease (CJD). A beta plaques are thought to be responsible for this decrease in AD patients, whereas such A beta plaques are rarely seen in CJD. To investigate the A beta pattern in brain and CSF of neuropathologically confirmed CJD and AD patients we used an electrophoretic method to investigate A beta peptide fractions which are not accessible to ELISA and immunohistochemistry. We analyzed A beta peptides in the CSF of autopsy-confirmed CJD and AD patients and the corresponding brain homogenates using a quantitative urea-based A beta electrophoresis immunoblot (A beta-SDS-PAGE/immunoblot).The CSF A beta 1-42 decrease correlated with the brain A beta load in AD, but not in CJD. There was no difference in the soluble fractions of brain homogenate in AD and CJD. We therefore conclude that different mechanisms in AD and CJD are responsible for the A beta 1-42 decrease in the CSF.
引用
收藏
页码:691 / 697
页数:7
相关论文
共 50 条
  • [21] Programmed cell death (apoptosis) in Alzheimer's disease and Creutzfeldt-Jakob disease
    Jesionek-Kupnicka, D
    Buczynski, J
    Kordek, R
    Sobow, T
    Kloszewska, I
    Papierz, W
    Liberski, PP
    FOLIA NEUROPATHOLOGICA, 1997, 35 (04): : 233 - 235
  • [22] CREUTZFELDT-JAKOB DISEASE
    JANOTA, I
    BRITISH MEDICAL JOURNAL, 1982, 285 (6338): : 375 - 375
  • [23] CREUTZFELDT-JAKOB DISEASE
    MATTHEWS, WB
    BRITISH MEDICAL JOURNAL, 1985, 291 (6493): : 483 - 483
  • [24] CREUTZFELDT-JAKOB DISEASE
    DELAHUNT, B
    ALEXANDER, WS
    NEW ZEALAND MEDICAL JOURNAL, 1982, 95 (720) : 806 - 809
  • [25] Can Creutzfeldt-Jakob disease unravel the mysteries of Alzheimer?
    Kovacs, Gabor G.
    PRION, 2016, 10 (05) : 369 - 376
  • [26] Creutzfeldt-Jakob Disease
    Narula, Reshma
    Tinaz, Sule
    NEW ENGLAND JOURNAL OF MEDICINE, 2018, 378 (04):
  • [27] CREUTZFELDT-JAKOB DISEASE
    KNIGHT, R
    BRITISH JOURNAL OF HOSPITAL MEDICINE, 1989, 41 (02): : 165 - &
  • [28] CREUTZFELDT-JAKOB DISEASE
    BAKER, HF
    RIDLEY, RM
    CROW, TJ
    BRITISH MEDICAL JOURNAL, 1985, 291 (6498): : 822 - 823
  • [29] Creutzfeldt-Jakob disease
    Finkelstein, LE
    Mendelson, MH
    Tejero, C
    Troccoli, J
    AMERICAN JOURNAL OF NURSING, 1998, 98 (09) : 66 - 67
  • [30] THE CREUTZFELDT-JAKOB DISEASE
    MEIER, C
    AKTUELLE NEUROLOGIE, 1980, 7 (02) : 75 - 86