Expression of the Neuronal Adaptor Protein X11 alpha Protects Against Memory Dysfunction in a Transgenic Mouse Model of Alzheimer's Disease

Jacqueline C. Mitchell; Michael S. Perkinton; Darran M. Yates; Kwok-Fai Lau; Boris Rogelj; Christopher C. J. Miller; Declan M. McLoughlin

doi:10.3233/JAD-2009-1341

Expression of the Neuronal Adaptor Protein X11 alpha Protects Against Memory Dysfunction in a Transgenic Mouse Model of Alzheimer's Disease

Jacqueline C. Mitchell, Michael S. Perkinton, Darran M. Yates, Kwok-Fai Lau, Boris Rogelj, Christopher C. J. Miller, Declan M. McLoughlin

Basic and Clinical Neuroscience

Research output: Contribution to journal › Article › peer-review

Abstract

X11 alpha is a neuronal-specific adaptor protein that binds to the amyloid-beta protein precursor (A beta PP). Overexpression of X11 alpha reduces A beta production but whether X11 alpha also protects against A beta-related memory dysfunction is not known. To test this possibility, we crossed X11 alpha transgenic mice with A beta PP-Tg2576 mice. A beta PP-Tg2576 mice produce high levels of brain A beta and develop age-related defects in memory function that correlate with increasing A beta load. Overexpression of X11 alpha alone had no detectable adverse effect upon behavior. However, X11 alpha reduced brain A beta levels and corrected spatial reference memory defects in aged X11 alpha/A beta PP double transgenics. Thus, X11 alpha may be a therapeutic target for Alzheimer's disease.

Original language	English
Pages (from-to)	31 - 36
Number of pages	6
Journal	JOURNAL OF ALZHEIMERS DISEASE
Volume	20
Issue number	1
DOIs	https://doi.org/10.3233/JAD-2009-1341
Publication status	Published - 2010

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title = "Expression of the Neuronal Adaptor Protein X11 alpha Protects Against Memory Dysfunction in a Transgenic Mouse Model of Alzheimer's Disease",

abstract = "X11 alpha is a neuronal-specific adaptor protein that binds to the amyloid-beta protein precursor (A beta PP). Overexpression of X11 alpha reduces A beta production but whether X11 alpha also protects against A beta-related memory dysfunction is not known. To test this possibility, we crossed X11 alpha transgenic mice with A beta PP-Tg2576 mice. A beta PP-Tg2576 mice produce high levels of brain A beta and develop age-related defects in memory function that correlate with increasing A beta load. Overexpression of X11 alpha alone had no detectable adverse effect upon behavior. However, X11 alpha reduced brain A beta levels and corrected spatial reference memory defects in aged X11 alpha/A beta PP double transgenics. Thus, X11 alpha may be a therapeutic target for Alzheimer's disease.",

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doi = "10.3233/JAD-2009-1341",

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T1 - Expression of the Neuronal Adaptor Protein X11 alpha Protects Against Memory Dysfunction in a Transgenic Mouse Model of Alzheimer's Disease

AU - Mitchell, Jacqueline C.

AU - Perkinton, Michael S.

AU - Yates, Darran M.

AU - Lau, Kwok-Fai

AU - Rogelj, Boris

AU - Miller, Christopher C. J.

AU - McLoughlin, Declan M.

PY - 2010

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AB - X11 alpha is a neuronal-specific adaptor protein that binds to the amyloid-beta protein precursor (A beta PP). Overexpression of X11 alpha reduces A beta production but whether X11 alpha also protects against A beta-related memory dysfunction is not known. To test this possibility, we crossed X11 alpha transgenic mice with A beta PP-Tg2576 mice. A beta PP-Tg2576 mice produce high levels of brain A beta and develop age-related defects in memory function that correlate with increasing A beta load. Overexpression of X11 alpha alone had no detectable adverse effect upon behavior. However, X11 alpha reduced brain A beta levels and corrected spatial reference memory defects in aged X11 alpha/A beta PP double transgenics. Thus, X11 alpha may be a therapeutic target for Alzheimer's disease.

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DO - 10.3233/JAD-2009-1341

M3 - Article

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SP - 31

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JO - JOURNAL OF ALZHEIMERS DISEASE

JF - JOURNAL OF ALZHEIMERS DISEASE

IS - 1

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Expression of the Neuronal Adaptor Protein X11 alpha Protects Against Memory Dysfunction in a Transgenic Mouse Model of Alzheimer's Disease

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