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Clinical Chemistry 51: 1650-1660, 2005. First published July 14, 2005; 10.1373/clinchem.2005.051201
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(Clinical Chemistry. 2005;51:1650-1660.)
© 2005 American Association for Clinical Chemistry, Inc.

Proteomics and Protein Markers

Amino-Truncated ß-Amyloid42 Peptides in Cerebrospinal Fluid and Prediction of Progression of Mild Cognitive Impairment

Hugo Vanderstichele1,a, Geert De Meyer1, Niels Andreasen2, Vesna Kostanjevecki1, Anders Wallin3, Annika Olsson4, Kaj Blennow4 and Eugeen Vanmechelen1

1 Innogenetics NV, Gent, Belgium.
2 Neurotec, Department of Geriatric Medicine, Huddinge University Hospital, Stockholm, Sweden.
3 Department of Clinical Neuroscience, Department of Psychiatry, Göteborg University, Mölndal, Sweden.
4 Department of Clinical Neuroscience, Experimental Neuroscience, Sahlgrenska University Hospital, Mölndal, Sweden.

aAddress correspondence to this author at: Industriepark Zwijnaarde 7, Box 4, B-9052 Gent, Belgium. Fax 32-9-241-0907; e-mail hugovdr{at}innogenetics.be.

Background: Early identification of patients with mild cognitive impairment (MCI) progressing to Alzheimer disease (MCI-AD) by use of biomarkers in cerebrospinal fluid (CSF) is an essential step toward improving clinical diagnosis and drug development. We evaluated whether different ß-amyloid42 (Aß42) peptides can add further information to the combined use of tau and Aß1–42 for predicting risk of progression of MCI to AD.

Methods: We used xMAP® technology to simultaneously quantify different Aß42 peptides modified at the amino terminus, tau, and phosphorylated tau (P-tau181P) in CSF. Aß42 peptide concentrations were measured by use of immunoreactivity toward Aß monoclonal antibodies [3D6 (Aß42-3D6), WO2 (Aß42-WO2), 6E10 (Aß42-6E10), and 4G8 (Aß42-4G8)]. The discriminant ability of the markers was evaluated by ROC curve analysis.

Results: The areas under the curves for the separation of MCI-AD from nonprogressing MCI (MCI-N) were significantly higher when we used Aß42-3D6/Aß42-WO2, Aß42-3D6/Aß42-6E10, or Aß42-3D6/Aß42-4G8 compared with Aß42-3D6. In addition, differentiation of MCI-N from MCI-AD was improved by quantification of full-length Aß1–42 (Aß42-3D6) compared with Aß42-WO2, Aß42-6E10, or Aß42-4G8. Several Aß42 peptides truncated at the amino terminus (Aß11–42 and Aß8–42) were identified in CSF by surface-enhanced laser desorption/ionization time-of-flight technology.

Conclusion: The CSF markers tau, Aß42 forms, and P-tau181P, when used as adjuncts to clinical diagnosis, have the potential to help identify AD pathology and could be a valuable asset for early AD diagnosis.




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