Email updates

Keep up to date with the latest news and content from BMC Neuroscience and BioMed Central.

This article is part of the supplement: Annual Meeting of the Study Group Neurochemistry. International Conference of the Gesellschaft für Biochemie und Molekularbiologie 2006 (GBM 2006): Molecular pathways in health and disease of the nervous system

Open Access Poster presentation

In vivo diagnosis and therapy of Alzheimer's disease

Katja Wiesehan*, Thomas van Groen, Reinhold P Linke, Stephan Patt and Dieter Willbold

  • * Corresponding author: Katja Wiesehan

Author Affiliations

IBI-2/INB, Forschungszentrum Jülich, 52425 Jülich, Germany, Juelich, Germany

For all author emails, please log on.

BMC Neuroscience 2007, 8(Suppl 1):P19  doi:10.1186/1471-2202-8-S1-P19

The electronic version of this article is the complete one and can be found online at:


Published:23 March 2007

© 2007 Wiesehan et al; licensee BioMed Central Ltd.

Poster presentation

Alzheimer's disease (AD) is a progessive neurodegenerative disorder. The 'amyloid cascade hypothesis' assigns the amyloid-beta-peptide (Abeta) a central role in the pathogenesis of Alzheimer's disease. We searched for peptides consisting of the D-enantiomers of amino acids (D-peptides) that bind to Abeta (1–42). D-peptides are thought to be protease resistant and less immunogenic than the respective L-enantiomers and can be identified by mirror image phage display. We carried out a screening of a randomized 12 mer peptide library and identified a dominating D-peptide (D-pep). In vitro experiments verified binding of D-pep to naturally occuring Abeta and showed positive influence of D-pep on Abeta cytotoxicity. In vivo experiments in transgenic mice suggest D-pep to cross the blood-brain-barrier and to reduce Abeta loads in the living brain.