Wnt/β-Catenin Signaling in Alzheimer's Disease
Giancarlo V. De Ferrari, Miguel E. Avila, Matias A. Medina, Eduardo Perez-Palma, Bernabe I. Bustos and Marcelo A. AlarconAffiliation:
Center for Biomedical Research and FONDAP Center for Genome Regulation, Universidad Andres Bello, Republica #239, PO Box 8370134, Santiago, Chile.
AbstractAlzheimer’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.
Alzheimer's disease, amyloid precursor protein, tau, apolipoprotein E, Wnt/β-catenin signaling, lithium.
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