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Reduction of Alzheimer’s Disease Amyloid Plaque Load in Transgenic Mice by D3, a D ‐Enantiomeric Peptide Identified by Mirror Image Phage Display
Author(s) -
van Groen Thomas,
Wiesehan Katja,
Funke Susanne A.,
Kadish Inga,
NagelSteger Luitgard,
Willbold Dieter
Publication year - 2008
Publication title -
chemmedchem
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.817
H-Index - 100
eISSN - 1860-7187
pISSN - 1860-7179
DOI - 10.1002/cmdc.200800273
Subject(s) - transgene , genetically modified mouse , in vivo , disease , peptide , amyloid (mycology) , enantiomer , in vitro , neuroscience , amyloid precursor protein , alzheimer's disease , biochemistry , chemistry , biology , medicine , genetics , pathology , stereochemistry , gene
Alzheimer's disease (AD) is a progressive neurodegenerative disorder, affecting more than 20 million people world‐wide. Only palliative therapies are available today. We identified a novel D ‐enantiomeric amino acid peptide “D3” with significant Aβ disaggregation and Aβ aggregation inhibiting properties in vitro an in vivo. It inhibits cytotoxicity in cell culture and reduces amyloid plaque load and cerebral damage of transgenic AD mouse models. D3 might be a tool for further research approaches on the origin of AD and might provide a novel basis for therapeutic and preventive approaches to AD.