Abstract
Alzheimer’s disease is a neurodegenerative disorder that causes a progressive decline of mental and cognitive processes such as memory, judgment and reasoning. We proposed earlier that a sustained loss of function of Wnt/β- catenin signaling components underlies the onset and progression of the disease. Here, we discuss recent data on the involvement of Wnt/b-catenin signaling on amyloid precursor protein (APP) processing, Aβ peptide neurotoxicity, τ phosphorylation, and modulation of Apolipoprotein E function in the brain. We conclude that several components of the cascade are actively engaged in the events leading to AD neuropathology and propose that compounds that mimic activation of this signaling cascade, such as lithium, should be considered for therapeutic intervention in Alzheimer's patients. In summary, data accumulated during the past decade confirm some important predictions of our hypothesis where components of this signaling cascade are actively engaged in the events leading to AD neuropathology and that compounds that mimic activation of this signaling cascade, such as lithium, should be considered for therapeutic intervention in Alzheimer's patients.
Keywords: Alzheimer's disease, amyloid precursor protein, tau, apolipoprotein E, Wnt/β-catenin signaling, lithium.
CNS & Neurological Disorders - Drug Targets
Title:Wnt/β-Catenin Signaling in Alzheimer's Disease
Volume: 13 Issue: 5
Author(s): Giancarlo V. De Ferrari, Miguel E. Avila, Matias A. Medina, Eduardo Perez-Palma, Bernabe I. Bustos and Marcelo A. Alarcon
Affiliation:
Keywords: Alzheimer's disease, amyloid precursor protein, tau, apolipoprotein E, Wnt/β-catenin signaling, lithium.
Abstract: Alzheimer’s disease is a neurodegenerative disorder that causes a progressive decline of mental and cognitive processes such as memory, judgment and reasoning. We proposed earlier that a sustained loss of function of Wnt/β- catenin signaling components underlies the onset and progression of the disease. Here, we discuss recent data on the involvement of Wnt/b-catenin signaling on amyloid precursor protein (APP) processing, Aβ peptide neurotoxicity, τ phosphorylation, and modulation of Apolipoprotein E function in the brain. We conclude that several components of the cascade are actively engaged in the events leading to AD neuropathology and propose that compounds that mimic activation of this signaling cascade, such as lithium, should be considered for therapeutic intervention in Alzheimer's patients. In summary, data accumulated during the past decade confirm some important predictions of our hypothesis where components of this signaling cascade are actively engaged in the events leading to AD neuropathology and that compounds that mimic activation of this signaling cascade, such as lithium, should be considered for therapeutic intervention in Alzheimer's patients.
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Cite this article as:
Ferrari V. De Giancarlo, Avila E. Miguel, Medina A. Matias, Perez-Palma Eduardo, Bustos I. Bernabe and Alarcon A. Marcelo, Wnt/β-Catenin Signaling in Alzheimer's Disease, CNS & Neurological Disorders - Drug Targets 2014; 13 (5) . https://dx.doi.org/10.2174/1871527312666131223113900
DOI https://dx.doi.org/10.2174/1871527312666131223113900 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
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