Presenilin transgenic mice as models of Alzheimer's disease.

Brain Structure & Function
Gregory A ElderPatrick R Hof

Abstract

Mutations in presenilin-1 (PS1) and presenilin-2 (PS2) cause familial Alzheimer's disease (FAD). Presenilins influence multiple molecular pathways and are best known for their role in the gamma-secretase cleavage of type I transmembrane proteins including the amyloid precursor protein (APP). PS1 and PS2 FAD mutant transgenic mice have been generated using a variety of promoters. PS1-associated FAD mutations have also been knocked into the endogenous mouse gene. PS FAD mutant mice consistently show elevations of Abeta42 with little if any effect on Abeta40. When crossed with plaque forming APP FAD mutant lines, the PS1 FAD mutants cause earlier and more extensive plaque deposition. Although single transgenic PS1 or PS2 mice do not form plaques, they exhibit a number of pathological features including age-related neuronal and synaptic loss as well as vascular pathology. They also exhibit increased susceptibility to excitotoxic injury most likely on the basis of exaggerated calcium release from the endoplasmic reticulum. Electrophysiologically long-term potentiation in the hippocampus is increased in young PS1 FAD mutant mice but this effect appears to be lost with aging. In most studies neurogenesis in the adult hippocampus is al...Continue Reading

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Citations

Oct 12, 2010·Journal of Neural Transmission·Brandon K HarveyMikko Airavaara
Feb 12, 2013·Brain Research Bulletin·Valérie ZuffereyArmand Savioz
Jan 5, 2011·PloS One·Brian P HeadHemal H Patel
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