Expression of the neuronal adaptor protein X11alpha protects against memory dysfunction in a transgenic mouse model of Alzheimer's disease.
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Authors
Mitchell, Jacqueline C
Perkinton, Michael S
Yates, Darran M
Lau, Kwok-Fai
Rogelj, Boris
Miller, Christopher C J
McLoughlin, Declan M
Issue Date
2010
Type
Journal Article
Research Support, Non-U.S. Gov't
Research Support, Non-U.S. Gov't
Language
en
Keywords
Alternative Title
Abstract
X11alpha is a neuronal-specific adaptor protein that binds to the amyloid-beta protein precursor (AbetaPP). Overexpression of X11alpha reduces Abeta production but whether X11alpha also protects against Abeta-related memory dysfunction is not known. To test this possibility, we crossed X11alpha transgenic mice with AbetaPP-Tg2576 mice. AbetaPP-Tg2576 mice produce high levels of brain Abeta and develop age-related defects in memory function that correlate with increasing Abeta load. Overexpression of X11alpha alone had no detectable adverse effect upon behavior. However, X11alpha reduced brain Abeta levels and corrected spatial reference memory defects in aged X11alpha/AbetaPP double transgenics. Thus, X11alpha may be a therapeutic target for Alzheimer's disease.
Description
Citation
Mitchell, J. C., Perkinton, M. S., Yates, D. M., Lau, K. F., Rogelj, B., Miller, C. C., & McLoughlin, D. M. (2010). Expression of the neuronal adaptor protein X11alpha protects against memory dysfunction in a transgenic mouse model of Alzheimer's disease. Journal of Alzheimer's disease : JAD, 20(1), 31–36. https://doi.org/10.3233/JAD-2009-1341
Publisher
License
Journal
Journal of Alzheimer's disease : JAD
Volume
20
Issue
1
PubMed ID
ISSN
1875-8908