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    The Endoplasmic Reticulum Stress Response in Neuroprogressive Diseases: Emerging Pathophysiological Role and Translational Implications

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    Author
    Morris, G; Puri, BK; Walder, K; Berk, M; Stubbs, B; Maes, M; Carvalho, AF
    Date
    2018-12-01
    Source Title
    Molecular Neurobiology
    Publisher
    SPRINGER
    University of Melbourne Author/s
    Berk, Michael
    Affiliation
    Psychiatry
    Metadata
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    Document Type
    Journal Article
    Citations
    Morris, G., Puri, B. K., Walder, K., Berk, M., Stubbs, B., Maes, M. & Carvalho, A. F. (2018). The Endoplasmic Reticulum Stress Response in Neuroprogressive Diseases: Emerging Pathophysiological Role and Translational Implications. MOLECULAR NEUROBIOLOGY, 55 (12), pp.8765-8787. https://doi.org/10.1007/s12035-018-1028-6.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/256290
    DOI
    10.1007/s12035-018-1028-6
    Abstract
    The endoplasmic reticulum (ER) is the main cellular organelle involved in protein synthesis, assembly and secretion. Accumulating evidence shows that across several neurodegenerative and neuroprogressive diseases, ER stress ensues, which is accompanied by over-activation of the unfolded protein response (UPR). Although the UPR could initially serve adaptive purposes in conditions associated with higher cellular demands and after exposure to a range of pathophysiological insults, over time the UPR may become detrimental, thus contributing to neuroprogression. Herein, we propose that immune-inflammatory, neuro-oxidative, neuro-nitrosative, as well as mitochondrial pathways may reciprocally interact with aberrations in UPR pathways. Furthermore, ER stress may contribute to a deregulation in calcium homoeostasis. The common denominator of these pathways is a decrease in neuronal resilience, synaptic dysfunction and even cell death. This review also discusses how mechanisms related to ER stress could be explored as a source for novel therapeutic targets for neurodegenerative and neuroprogressive diseases. The design of randomised controlled trials testing compounds that target aberrant UPR-related pathways within the emerging framework of precision psychiatry is warranted.

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