Paul Leibowitz

TL;DR: Transgenic mice that express high levels of human mutant APP support a primary role for APP/Aβ in the genesis of AD and could provide a preclinical model for testing therapeutic drugs.

TL;DR: In this paper, the authors describe the construction of transgenic animal models for testing potential treatments for Alzheimer's disease, based on expression of all three forms of the β-amyloid precursor protein (APP), APP 695, APP 751, and APP 770 ), as well as various point mutations based on naturally occurring mutations, such as the London and Indiana familial Alzheimer disease (FAD) mutations at amino acid 717, and predicted mutations in the APP gene.

TL;DR: Results extend to rabbits the authors' previous observation that this transgene contains the sequence elements required for high‐level expression in the appropriate cells of transgenic mice, and suggest that the hCD4 transgenic rabbits described herein will have an increased susceptibility to HIV‐1 infection.

TL;DR: In this article, the authors describe the construction of transgenic mouse models for testing potential treatments for Alzheimer's disease, based on expression of all three forms of the β-amyloid precursor protein (APP), APP 695, APP 751, and APP 770 ), as well as various point mutations based on naturally occurring mutations, such as the London and Indiana familial Alzheimer's Disease (FAD) mutations at amino acid 717, and predicted mutations in the APP gene.

TL;DR: In this article, a method for treating cells with E19 protein in order to alter the presentation of MHC class I cell surface antigens on these cells and thereby allow introduction of these cells into a recipient organism while reducing transplant rejection by the recipient organism's immune system is described.