Antje Willuweit, Joachim Velden, Robert Godemann, Andre Manook, Fritz Jetzek, Hartmut Tintrup, Gunther Kauselmann, Branko Zevnik, Gjermund Henriksen, Alexander Drzezga, Johannes Pohlner, Michael Schoor, John A. Kemp, Heinz von der Kammer

Transgenic mice expressing mutated amyloid precursor protein (APP) and presenilin (PS)-1 or -2 have been successfully used to model cerebral beta-amyloidosis, one of the characteristic hallmarks of Alzheimer's disease (AD) pathology. However, the use of many transgenic lines is limited by premature death, low breeding efficiencies and late onset and high inter-animal variability of the pathology, creating a need for improved animal models. Here we describe the detailed characterization of a new homozygous double-transgenic mouse line that addresses most of these issues.