Reduced CSF carboxyterminally truncated Aβ peptides in frontotemporal lobe degenerations

被引:32
作者
Bibl, M.
Mollenhauer, B.
Wolf, S.
Esselmann, H.
Lewczuk, P.
Kornhuber, J.
Wiltfang, J.
机构
[1] Univ Erlangen Nurnberg, Dept Psychiat & Psychotherapy, Mol Neurobiol Lab, D-91054 Erlangen, Germany
[2] Harvard Univ, Sch Med, Brigham & Womens Hosp, Ctr Neurol Dis, Boston, MA USA
[3] Univ Gottingen, Dept Psychiat, Gottingen, Germany
关键词
Alzheimer's disease; frontotemporal degeneration; cerebrospinal fluid; amyloid-beta peptides; biomarkers;
D O I
10.1007/s00702-006-0618-z
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Cerebrospinal fluid (CSF) carboxyterminally truncated amyloid-beta (A beta) peptides, A beta 1-42 and tau protein were evaluated in 30 patients with frontotemporal lobe degenerations (FTLD), 30 Alzheimer's disease (AD) patients and 30 non-demented disease controls (NDC) by A beta-SDS-PAGE/immunoblot as well as commercial ELISAs for A beta 1-42 and total tau. FTLD displayed a significant drop of A beta 1-37 (p = 2.7 x 10(-4)), A beta 1-38 (p = 4.2 x 10(-5)) and A beta 1-42 (p = 3.3 x 10(-4)). A beta 1-42 was selectively decreased in AD (p = 8.5 x 10(-1)). Decreased A beta 1-38 enabled contrasts of beyond 85% to distinguish FTLD from AD and NDC patients, alone or in combination. Accordingly, low CSF A beta 1-37 and A beta 1-38 represent a biomarker candidate for FTLD and may reflect disease-specific changes of APP metabolism. Further validation should be carried out on dementias other than AD, diagnostically relevant control groups without dementia and without any evident affection of the central nervous system and subgroups of FTLD. Moreover, independent methods of measurement should be applied to CSF A beta 1-38.
引用
收藏
页码:621 / 628
页数:8
相关论文
共 34 条
  • [31] Consensus paper of the WFSBP Task Force on biological markers of dementia:: The role of CSF and blood analysis in the early and differential diagnosis of dementia
    Wiltfang, J
    Lewczuk, P
    Riederer, P
    Grünblatt, E
    Hock, C
    Scheltens, P
    Hampel, H
    Vanderstichele, H
    Iqbal, K
    Galasko, D
    Lannfelt, L
    Otto, M
    Esselmann, H
    Henkel, AW
    Kornhuber, J
    Blennow, K
    [J]. WORLD JOURNAL OF BIOLOGICAL PSYCHIATRY, 2005, 6 (02) : 69 - 84
  • [32] β-Amyloid peptides in cerebrospinal fluid of patients with Creutzfeldt-Jakob disease
    Wiltfang, J
    Esselmann, H
    Smirnov, A
    Bibl, M
    Cepek, L
    Steinacker, P
    Mollenhauer, B
    Buerger, K
    Hampel, H
    Paul, S
    Neumann, M
    Maler, M
    Zerr, I
    Kornhuber, J
    Kretzschmar, HA
    Poser, S
    Otto, M
    [J]. ANNALS OF NEUROLOGY, 2003, 54 (02) : 263 - 267
  • [33] Highly conserved and disease-specific patterns of carboxyterminally truncated Aβ peptides 1-37/38/39 in addition to 1-40/42 in Alzheimer's disease and in patients with chronic neuroinflammation
    Wiltfang, J
    Esselmann, H
    Bibl, M
    Smirnov, A
    Otto, M
    Paul, S
    Schmidt, B
    Klafki, HW
    Maler, M
    Dyrks, T
    Bienert, M
    Beyermann, M
    Rüther, E
    Kornhuber, J
    [J]. JOURNAL OF NEUROCHEMISTRY, 2002, 81 (03) : 481 - 496
  • [34] Elevation of β-amyloid peptide 2-42 in sporadic and familial Alzheimer's disease and its generation in PS1 knockout cells
    Wiltfang, J
    Esselmann, H
    Cupers, P
    Neumann, M
    Kretzschmar, H
    Beyermann, M
    Schleuder, D
    Jahn, H
    Rüther, E
    Kornhuber, J
    Annaert, W
    De Strooper, B
    Saftig, P
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (46) : 42645 - 42657