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    SFRP-mediated Wnt sequestration as a potential therapeutic target for Alzheimer's disease

    240101_240101 .pdf (309.1Kb)
    Access Status
    Open access
    Authors
    Warrier, Sudha
    Marimuthu, R.
    Sekhar, S.
    Bhuvanalakshmi, G.
    Arfuso, Frank
    Das, A.
    Bhonde, R.
    Martins, R.
    Dharmarajan, Arunasalam
    Date
    2016
    Type
    Journal Article
    
    Metadata
    Show full item record
    Citation
    Warrier, S. and Marimuthu, R. and Sekhar, S. and Bhuvanalakshmi, G. and Arfuso, F. and Das, A. and Bhonde, R. et al. 2016. SFRP-mediated Wnt sequestration as a potential therapeutic target for Alzheimer's disease. International Journal of Biochemistry and Cell Biology. 75: pp. 104-111.
    Source Title
    International Journal of Biochemistry and Cell Biology
    DOI
    10.1016/j.biocel.2016.04.002
    ISSN
    1357-2725
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/30058
    Collection
    • Curtin Research Publications
    Abstract

    The extracellular ligand, Wnt, and its receptors are involved in sign al transduction and play an important role in axis formation and neural development. In neurodegenerative disorders such as Alzheimer's disease (AD), a decrease of the intracellular Wnt effector, ß-catenin, has been linked to amyloid-ß-peptide-induced neurotoxicity. Despite this knowledge, targeting Wnt inhibitors as potential biomarkers has not been explored, and harnessing Wnt activators as therapeutic candidates remains largely not investigated. A wide acting family of Wnt mediators, secreted frizzled-related proteins (sFRPs), has not been probed so far as molecular indicators of disease occurrence and progression of Alzheimer's. Unlike the effect of the Dickkopf (DKK) family of Wnt antagonists on AD, the sFRP molecules have a more pleiotropic impact on the Wnt signaling cascade and probably have a far-reaching involvement in neurodegeneration. The role of sFRPs has been poorly described in AD, and in this review, we analyze the present status of the role of sFRPs on neurodegeneration, their likely involvement, and potential implications in treatment modalities of AD. This information would provide valuable clues for the development of potential therapeutic targets for aberrant neurodegenerative disorders.

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