Expression of the neuronal adaptor protein X11alpha protects against memory dysfunction in a transgenic mouse model of Alzheimer's disease.
AuthorsMitchell, Jacqueline C
Perkinton, Michael S
Yates, Darran M
Miller, Christopher C J
McLoughlin, Declan M
AffiliationMRC Centre for Neurodegeneration Research, King's College London, Institute of Psychiatry, London, UK.
MeSHAdaptor Proteins, Signal Transducing
Amyloid beta-Protein Precursor
Analysis of Variance
Disease Models, Animal
Nerve Tissue Proteins
MetadataShow full item record
CitationExpression 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.
JournalJournal of Alzheimer's disease : JAD
AbstractX11alpha 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.
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