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   <subfield code="a">10.1007/s00702-006-0485-7</subfield>
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   <subfield code="a">Cerebrospinal fluid diagnostic markers correlate with lower plasma copper and ceruloplasmin in patients with Alzheimer's disease</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[H. Kessler, F.-G. Pajonk, P. Meisser, T. Schneider-Axmann, K.-H. Hoffmann, T. Supprian, W. Herrmann, R. Obeid, G. Multhaup, P. Falkai, T. A. Bayer]</subfield>
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   <subfield code="a">Summary.: Increasing evidence links Alzheimer's disease (AD) with misbalanced Cu homeostasis. Recently, we have shown that dietary Cu supplementation in a transgenic mouse model for AD increases bioavailable brain Cu levels, restores Cu, Zn-super oxide-1 activity, prevents premature death, and lowers Aβ levels. In the present report we investigated AD patients with normal levels of Aβ42, Tau and Phospho-Tau in the cerebrospinal fluid (CSF) in comparison with AD patients exhibiting aberrant levels in these CSF biomarkers. The influence of these cerebrospinal fluid (CSF) diagnostic markers with primary dependent variables blood Cu, Zn and ceruloplasmin (CB) and secondary with CSF profiles of Cu, Zn and neurotransmitters was determined. Multivariate tests revealed a significant effect of factor diagnostic group (no AD diagnosis in CSF or AD diagnosis in CSF) for variables plasma Cu and CB (F = 4.80; df = 2, 23; p = 0.018). Subsequent univariate tests revealed significantly reduced plasma Cu (−12.7%; F = 7.05; df = 1, 25; p = 0.014) and CB (−14.1%; F = 9.44; df = 1, 24; p = 0.005) levels in patients with aberrant CSF biomarker concentrations. Although only AD patients were included, the reduced plasma Cu and CB levels in patients with a CSF diagnosis of advanced AD supports previous observations that a mild Cu deficiency might contribute to AD progression.</subfield>
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   <subfield code="a">Springer-Verlag, 2006</subfield>
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   <subfield code="a">Keywords: CSF, copper, Alzheimer's disease</subfield>
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   <subfield code="a">Kessler</subfield>
   <subfield code="D">H.</subfield>
   <subfield code="u">Department of Psychiatry and Psychotherapy, Saarland University, Homburg/Saar, Germany</subfield>
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   <subfield code="a">Pajonk</subfield>
   <subfield code="D">F.-G</subfield>
   <subfield code="u">Department of Psychiatry and Psychotherapy, Saarland University, Homburg/Saar, Germany</subfield>
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   <subfield code="a">Meisser</subfield>
   <subfield code="D">P.</subfield>
   <subfield code="u">Department of Psychiatry and Psychotherapy, Saarland University, Homburg/Saar, Germany</subfield>
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   <subfield code="a">Schneider-Axmann</subfield>
   <subfield code="D">T.</subfield>
   <subfield code="u">Department of Psychiatry and Psychotherapy, Saarland University, Homburg/Saar, Germany</subfield>
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   <subfield code="a">Hoffmann</subfield>
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   <subfield code="u">Department of Psychiatry and Psychotherapy, Saarland University, Homburg/Saar, Germany</subfield>
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   <subfield code="a">Supprian</subfield>
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   <subfield code="u">Department of Psychiatry and Psychotherapy, Saarland University, Homburg/Saar, Germany</subfield>
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   <subfield code="u">Department for Clinical Chemistry, Central Laboratory, Saarland University Hospital, Homburg/Saar, Germany</subfield>
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   <subfield code="a">Obeid</subfield>
   <subfield code="D">R.</subfield>
   <subfield code="u">Department for Clinical Chemistry, Central Laboratory, Saarland University Hospital, Homburg/Saar, Germany</subfield>
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   <subfield code="a">Multhaup</subfield>
   <subfield code="D">G.</subfield>
   <subfield code="u">Institute for Chemistry-Biochemistry, Free University of Berlin, Berlin, Germany</subfield>
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   <subfield code="a">Falkai</subfield>
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   <subfield code="u">Department of Psychiatry and Psychotherapy, Saarland University, Homburg/Saar, Germany</subfield>
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   <subfield code="u">Department of Psychiatry and Psychotherapy, Saarland University, Homburg/Saar, Germany</subfield>
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   <subfield code="t">Journal of Neural Transmission</subfield>
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   <subfield code="g">113/11(2006-11-01), 1763-1769</subfield>
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