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      Wnt Signaling Deregulation in the Aging and Alzheimer’s Brain

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          Abstract

          Growing evidence suggests that synaptic signaling is compromised in the aging brain and in Alzheimer’s disease (AD), contributing to synaptic decline. Wnt signaling is a prominent pathway at the synapse and is required for synaptic plasticity and maintenance in the adult brain. In this review, we summarize the current knowledge on deregulation of Wnt signaling in the context of aging and AD. Emerging studies suggest that enhancing Wnt signaling could boost synaptic function during aging, and ameliorate synaptic pathology in AD. Although further research is needed to determine the precise contribution of deficient Wnt signaling to AD pathogenesis, targeting Wnt signaling components may provide novel therapeutic avenues for synapse protection or restoration in the brain.

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          Most cited references48

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          Neural mechanisms of ageing and cognitive decline.

          Nicholas A. Bishop, Tao Lu, Bruce A. Yankner (2010)
          During the past century, treatments for the diseases of youth and middle age have helped raise life expectancy significantly. However, cognitive decline has emerged as one of the greatest health threats of old age, with nearly 50% of adults over the age of 85 afflicted with Alzheimer's disease. Developing therapeutic interventions for such conditions demands a greater understanding of the processes underlying normal and pathological brain ageing. Recent advances in the biology of ageing in model organisms, together with molecular and systems-level studies of the brain, are beginning to shed light on these mechanisms and their potential roles in cognitive decline.
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            Wnt/Ca2+ signaling pathway: a brief overview.

            Antara De (2011)
            The non-canonical Wnt/Ca(2+) signaling cascade is less characterized than their canonical counterpart, the Wnt/β-catenin pathway. The non-canonical Wnt signaling pathways are diverse, defined as planer cell polarity pathway, Wnt-RAP1 signaling pathway, Wnt-Ror2 signaling pathway, Wnt-PKA pathway, Wnt-GSK3MT pathway, Wnt-aPKC pathway, Wnt-RYK pathway, Wnt-mTOR pathway, and Wnt/calcium signaling pathway. All these pathways exhibit a considerable degree of overlap between them. The Wnt/Ca(2+) signaling pathway was deciphered as a crucial mediator in development. However, now there is substantial evidence that the signaling cascade is involved in many other molecular phenomena. Many aspects of Wnt/Ca(2+) pathway are yet enigmatic. This review will give a brief overview of the fundamental and evolving concepts of the Wnt/Ca(2+) signaling pathway.
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              Synaptic Impairment in Alzheimer's Disease: A Dysregulated Symphony.

              Stefânia Forner, David Baglietto-Vargas, Alessandra C Martini … (2017)
              Alzheimer's disease (AD) is characterized by memory loss, cognitive decline, and devastating neurodegeneration, not only as a result of the extracellular accumulation of beta-amyloid peptide (Aβ) and intracellular accumulation of tau, but also as a consequence of the dysfunction and loss of synapses. Although significant advances have been made in our understanding of the relationship of the pathological role of Aβ and tau in synapse dysfunction, several questions remain as to how Aβ and tau interdependently cause impairments in synaptic function in AD. Overall, more insight into these questions should enable researchers in this field to develop novel therapeutic targets to mitigate or delay the cognitive deficits associated with this devastating disease.
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                Author and article information

                Contributors
                Journal
                Journal ID (nlm-ta): Front Cell Neurosci
                Journal ID (iso-abbrev): Front Cell Neurosci
                Journal ID (publisher-id): Front. Cell. Neurosci.
                Title: Frontiers in Cellular Neuroscience
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 1662-5102
                Publication date (Electronic): 22 May 2019
                Publication date Collection: 2019
                Volume: 13
                Electronic Location Identifier: 227
                Affiliations
                Department of Cell and Developmental Biology, University College London , London, United Kingdom
                Author notes

                Edited by: Lavinia Alberi, SICHH, Switzerland

                Reviewed by: Claire S. Durrant, University of Cambridge, United Kingdom; Paola Bovolenta, Spanish National Research Council (CSIC), Spain

                *Correspondence: Ernest Palomer, e.palomer@ 123456ucl.ac.uk Patricia C. Salinas, p.salinas@ 123456ucl.ac.uk

                †Co-first authors

                This article was submitted to Cellular Neuropathology, a section of the journal Frontiers in Cellular Neuroscience

                Article
                DOI: 10.3389/fncel.2019.00227
                PMC ID: 6538920
                PubMed ID: 31191253
                SO-VID: 5e798bf7-2918-4233-8b96-2485e8b590aa
                Copyright © Copyright © 2019 Palomer, Buechler and Salinas.
                License:

                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) and the copyright owner(s) 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.

                History
                Date received : 16 November 2018
                Date accepted : 06 May 2019
                Page count
                Figures: 2, Tables: 0, Equations: 0, References: 62, Pages: 8, Words: 0
                Categories
                Subject: Neuroscience
                Subject: Mini Review

                ScienceOpen disciplines: Neurosciences
                Keywords: wnt,aging brain,synapse degeneration,synaptic maintenance,alzheimer’s disease
                Data availability:
                ScienceOpen disciplines: Neurosciences
                Keywords: wnt, aging brain, synapse degeneration, synaptic maintenance, alzheimer’s disease

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