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Wnts in adult brain: from synaptic plasticity to cognitive deficiencies

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      Abstract

      During development of the central nervous system the Wnt signaling pathway has been implicated in a wide spectrum of physiological processes, including neuronal connectivity and synapse formation. Wnt proteins and components of the Wnt pathway are expressed in the brain since early development to the adult life, however, little is known about its role in mature synapses. Here, we review evidences indicating that Wnt proteins participate in the remodeling of pre- and post-synaptic regions, thus modulating synaptic function. We include the most recent data in the literature showing that Wnts are constantly released in the brain to maintain the basal neural activity. Also, we review the evidences that involve components of the Wnt pathway in the development of neurological and mental disorders, including a special emphasis on in vivo studies that relate behavioral abnormalities to deficiencies in Wnt signaling. Finally, we include the evidences that support a neuroprotective role of Wnt proteins in Alzheimer’s disease. We postulate that deregulation in Wnt signaling might have a fundamental role in the origin of neurological diseases, by altering the synaptic function at stages where the phenotype is not yet established but when the cognitive decline starts.

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      Most cited references 228

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      Wnt/β-catenin signaling and disease.

      The WNT signal transduction cascade controls myriad biological phenomena throughout development and adult life of all animals. In parallel, aberrant Wnt signaling underlies a wide range of pathologies in humans. In this Review, we provide an update of the core Wnt/β-catenin signaling pathway, discuss how its various components contribute to disease, and pose outstanding questions to be addressed in the future. Copyright © 2012 Elsevier Inc. All rights reserved.
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        Wnt/beta-catenin signaling: components, mechanisms, and diseases.

        Signaling by the Wnt family of secreted glycolipoproteins via the transcriptional coactivator beta-catenin controls embryonic development and adult homeostasis. Here we review recent progress in this so-called canonical Wnt signaling pathway. We discuss Wnt ligands, agonists, and antagonists, and their interactions with Wnt receptors. We also dissect critical events that regulate beta-catenin stability, from Wnt receptors to the cytoplasmic beta-catenin destruction complex, and nuclear machinery that mediates beta-catenin-dependent transcription. Finally, we highlight some key aspects of Wnt/beta-catenin signaling in human diseases including congenital malformations, cancer, and osteoporosis, and discuss potential therapeutic implications.
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          The Wnt signaling pathway in development and disease.

          Tight control of cell-cell communication is essential for the generation of a normally patterned embryo. A critical mediator of key cell-cell signaling events during embryogenesis is the highly conserved Wnt family of secreted proteins. Recent biochemical and genetic analyses have greatly enriched our understanding of how Wnts signal, and the list of canonical Wnt signaling components has exploded. The data reveal that multiple extracellular, cytoplasmic, and nuclear regulators intricately modulate Wnt signaling levels. In addition, receptor-ligand specificity and feedback loops help to determine Wnt signaling outputs. Wnts are required for adult tissue maintenance, and perturbations in Wnt signaling promote both human degenerative diseases and cancer. The next few years are likely to see novel therapeutic reagents aimed at controlling Wnt signaling in order to alleviate these conditions.
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            Author and article information

            Affiliations
            1Centro de Envejecimiento y Regeneración, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile Santiago, Chile
            2Departamento de Biologïa Celular y Molecular, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile Santiago, Chile
            Author notes

            Edited by: Lavinia Alberi, University of Fribourg, Switzerland

            Reviewed by: Urs Albrecht, University of Fribourg, Switzerland; Kerry Lee Tucker, University of Heidelberg, Germany

            *Correspondence: Nibaldo C. Inestrosa, Centro de Envejecimiento y Regeneración, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, P.O. Box 114-D, Santiago, Chile e-mail: ninestrosa@ 123456bio.puc.cl

            This article was submitted to the journal Frontiers in Cellular Neuroscience.

            Journal
            Front Cell Neurosci
            Front Cell Neurosci
            Front. Cell. Neurosci.
            Frontiers in Cellular Neuroscience
            Frontiers Media S.A.
            1662-5102
            03 December 2013
            2013
            : 7
            3847898
            10.3389/fncel.2013.00224
            Copyright © 2013 Oliva, Vargas and Inestrosa.

            This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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            Figures: 2, Tables: 0, Equations: 0, References: 228, Pages: 16, Words: 0
            Categories
            Neuroscience
            Review Article

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