Expression of the neuronal adaptor protein X11alpha protects against memory dysfunction in a transgenic mouse model of Alzheimer's disease.
Authors
Mitchell, Jacqueline CPerkinton, Michael S
Yates, Darran M
Lau, Kwok-Fai
Rogelj, Boris
Miller, Christopher C J
McLoughlin, Declan M
Affiliation
MRC Centre for Neurodegeneration Research, King's College London, Institute of Psychiatry, London, UK.Issue Date
2010MeSH
Adaptor Proteins, Signal TransducingAge Factors
Alzheimer Disease
Amyloid beta-Peptides
Amyloid beta-Protein Precursor
Analysis of Variance
Animals
Disease Models, Animal
Humans
Maze Learning
Memory Disorders
Mice
Mice, Transgenic
Nerve Tissue Proteins
Metadata
Show full item recordCitation
Expression of the neuronal adaptor protein X11alpha protects against memory dysfunction in a transgenic mouse model of Alzheimer's disease. 2010, 20 (1):31-6 J. Alzheimers Dis.Journal
Journal of Alzheimer's disease : JADDOI
10.3233/JAD-2009-1341PubMed ID
20378958Abstract
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.Item Type
ArticleLanguage
enISSN
1875-8908ae974a485f413a2113503eed53cd6c53
10.3233/JAD-2009-1341