Organiser's Note: The presenter of this talk withheld their permission for video to be published.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder, affecting more than 20 million people world-wide. Aging is the main risk factor of AD. Today, only palliative therapies for AD are available. Several lines of evidence, including genetics, have provided strong evidence for a central role of amyloid-β-peptide (Aβ) in the pathogenesis of AD. Recent studies indicate that soluble Aβ oligomers instead of fibrillar forms are the major toxic species. We report on a novel D-enantiomeric amino acid peptide which reduces amyloid plaque load and cerebral damage of transgenic mouse models of AD after direct brain application. Additionally, we show that next to plaque load and inflammation reduction, oral application of the peptide improves cognitive performance. We are providing in vitro data suggesting an Aβ42 oligomer modulating activity of D3. Next to its therapeutical interesting properties, D3 may help to elucidate the pathologic mechanisms underlying AD.

Van Groen T., Wiesehan K., Funke SA., Kadish I., Nagel-Steger L., Willbold D. (2008) Reduction of Alzheimer's Disease Amyloid Plaque Load in Transgenic Mice by D3, a D-Enantiomeric Peptide Identified by Mirror Image Phage Display. ChemMedChem. 3, 1848-1852.

Van Groen T., Kadish I., Wiesehan K., Funke S.A., Willbold D. (2009) In vitro and in vivo staining characteristics of small, fluorescent, Aβ42 binding D-enantiomeric peptides in transgenic AD mouse models. ChemMedChem 4, 276-282.