Affiliations: [a] Paracelsus-Elena Klinik Kassel and Departments of Neurology and Clinical Neurophysiology, Georg-August University, Göttingen, Germany | [b] Department of Psychiatry and Psychotherapy, University of Duisburg-Essen, Essen, Germany | [c] Georg-August University of Goettingen, Institute for Neuropathology, Göttingen, Germany | [d] Ludwig-Maximilians University, Institute for Neuropathology, Munich, Germany | [e] University of Ulm, Institute for Neurology, Ulm, Germany | [f] Department of Psychiatry, Psychotherapy and Addiction Medicine, Kliniken Essen-Mitte; University of Duisburg-Essen, Essen, Germany
Correspondence:
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Correspondence to: PD Dr. Brit Mollenhauer, Paracelsus-Elena Klinik Kassel and Departments of Neurology and Clinical Neurophysiology, Georg-August University, Göttingen, Germany. Tel.: +49 561 6009 107; E-mail: [email protected]. PD Dr. Mirko Bibl, Department of Psychiatry, Psychotherapy and Addiction Medicine, Kliniken Essen-Mitte, University of Duisburg-Essen, Henricistrasse 92, 45136 Essen, Germany. Tel.: +49 0201 17430046; E-mail: [email protected].
Abstract: Appropriate treatment of dementia requires biomarkers that provide an exact and differential diagnosis. We recently presented differentially expressed amyloid-β (Aβ) peptide patterns in cerebrospinal fluid (CSF) as biomarker candidates for neurochemical diagnosis of Alzheimer's disease (AD) and dementia with Lewy bodies (DLB). The objective of the present study was to investigate CSF Aβ peptide patterns in both neuropathologically and clinically defined diagnostic groups of AD and DLB. Using the quantitative Aβ-SDS-PAGE/immunoblot, we analyzed CSF samples of neuropathologically defined patients with AD (definite AD, dAD; n = 11) and DLB (definite, dDLB; n = 12). We compared absolute and relative quantities of CSF Aβ-peptides with a larger cohort of clinically diagnosed patients with probable AD (pAD; n = 71), probable DLB (pDLB; n = 32), and non-demented controls (NDC; n = 71). Each neuropathologically and clinically defined diagnostic group showed a similar relative distribution of CSF Aβ-peptides (Aβ1-X%. Aβ1-42% was lowered in dAD compared to NDC (p = 1.6 × 10−7, but did not differ between dAD and pAD. Aβ1-40ox% was elevated in dDLB as compared to NDC (p = 1.8 × 10−5, but did not differ between dDLB and pDLB. Thus, we were able to confirm previous results on Aβ peptide patterns in neuropathologically characterized patients with AD and DLB. Our results underline the usefulness of the CSF Aβ1-42% and Aβ1-40ox% as diagnostic biomarkers for AD and DLB, respectively.
