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Article
Caspase Cleavage of the Amyloid Precursor Protein is Prevented After Overexpression of Bcl-2 in a Triple Transgenic Mouse Model of Alzheimer’s Disease
International Journal of Physiology, Pathophysiology and Pharmacology
  • Debra K. Kumasaka, Boise State University
  • Veronica Galvan, Buck Institute for Age Research
  • Elizabeth Head, University of California - Irvine
  • Troy T. Rohn, Boise State University
Document Type
Article
Publication Date
1-1-2009
Disciplines
Abstract
A recent study demonstrated the lack of beta-amyloid (Aβ) plaque formation and accumulation of the amyloid precursor protein (APP) in a triple transgenic mouse model of Alzheimer’s disease (3xTg-AD) following overexpression of the anti-apoptotic protein, Bcl-2 (Rohn et al., J. Neurosci. 28: 3051-9, 2008). The supposition from that study was the accumulation of APP resulted from a decrease in caspase-mediated processing of APP. To determine a direct role for the caspase-cleavage of APP in 3xTg-AD mice, we designed a site-directed caspasecleavage antibody to APP and demonstrated it is a specific marker for caspase-cleaved APP. Application of this antibody revealed neuronal staining in the hippocampus and subiculum of 3xTg-AD mice. These results were confirmed utilizing a similar site-directed antibody to caspase-cleaved APP (APPneo). The caspase cleavage of APP as well as the formation of extracellular Aβ plaques was prevented in 3xTg-AD animals overexpressing Bcl-2. These results provide further support that caspases play a proximal role in promoting the pathology associated with AD.
Copyright Statement

This document was originally published by e-Century Publishing in International Journal of Physiology, Pathophysiology and Pharmacology. Copyright restrictions may apply. URL: http://www.ijppp.org/files/IJPPP901001.pdf

Citation Information
Debra K. Kumasaka, Veronica Galvan, Elizabeth Head and Troy T. Rohn. "Caspase Cleavage of the Amyloid Precursor Protein is Prevented After Overexpression of Bcl-2 in a Triple Transgenic Mouse Model of Alzheimer’s Disease" International Journal of Physiology, Pathophysiology and Pharmacology (2009)
Available at: http://works.bepress.com/troy_rohn/15/