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      The emerging role of exosomes in mental disorders

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Exosomes are a class of extracellular vesicles of endocytic origin, which are released by cells and are accessible in biofluids, such as saliva, urine, and plasma. These vesicles are enriched with small RNA, and they play a role in many physiological processes. In the brain, they are involved in processes including synaptic plasticity, neuronal stress response, cell-to-cell communication and neurogenesis. While exosomes have been implicated previously in cancer and neurodegenerative diseases, research regarding their role in mental disorders remains scarce. Given their functional significance in the brain, investigation in this field is warranted. Additionally, because exosomes can cross the blood–brain barrier, they may serve as accessible biomarkers of neural dysfunction. Studying exosomes may provide information towards diagnosis and therapeutic intervention, and specifically those derived from the brain may provide a mechanistic view of the disease phenotype. This review will discuss the roles of exosomes in the brain, and relate novel findings to current insights into mental disorders.

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          The gut-brain axis: interactions between enteric microbiota, central and enteric nervous systems

          Marilia Carabotti, Annunziata Scirocco, Maria Maselli … (2015)
          The gut-brain axis (GBA) consists of bidirectional communication between the central and the enteric nervous system, linking emotional and cognitive centers of the brain with peripheral intestinal functions. Recent advances in research have described the importance of gut microbiota in influencing these interactions. This interaction between microbiota and GBA appears to be bidirectional, namely through signaling from gut-microbiota to brain and from brain to gut-microbiota by means of neural, endocrine, immune, and humoral links. In this review we summarize the available evidence supporting the existence of these interactions, as well as the possible pathophysiological mechanisms involved. Most of the data have been acquired using technical strategies consisting in germ-free animal models, probiotics, antibiotics, and infection studies. In clinical practice, evidence of microbiota-GBA interactions comes from the association of dysbiosis with central nervous disorders (i.e. autism, anxiety-depressive behaviors) and functional gastrointestinal disorders. In particular, irritable bowel syndrome can be considered an example of the disruption of these complex relationships, and a better understanding of these alterations might provide new targeted therapies.
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            Synaptic plasticity and depression: new insights from stress and rapid-acting antidepressants.

            Ronald S. Duman, George Aghajanian, Gerard Sanacora … (2016)
            Depression is a common, devastating illness. Current pharmacotherapies help many patients, but high rates of a partial response or no response, and the delayed onset of the effects of antidepressant therapies, leave many patients inadequately treated. However, new insights into the neurobiology of stress and human mood disorders have shed light on mechanisms underlying the vulnerability of individuals to depression and have pointed to novel antidepressants. Environmental events and other risk factors contribute to depression through converging molecular and cellular mechanisms that disrupt neuronal function and morphology, resulting in dysfunction of the circuitry that is essential for mood regulation and cognitive function. Although current antidepressants, such as serotonin-reuptake inhibitors, produce subtle changes that take effect in weeks or months, it has recently been shown that treatment with new agents results in an improvement in mood ratings within hours of dosing patients who are resistant to typical antidepressants. Within a similar time scale, these new agents have also been shown to reverse the synaptic deficits caused by stress.
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              Tumor-Derived Exosomes and Their Role in Cancer Progression.

              Theresa L Whiteside (2016)
              Tumor cells actively produce, release, and utilize exosomes to promote tumor growth. Mechanisms through which tumor-derived exosomes subserve the tumor are under intense investigation. These exosomes are information carriers, conveying molecular and genetic messages from tumor cells to normal or other abnormal cells residing at close or distant sites. Tumor-derived exosomes are found in all body fluids. Upon contact with target cells, they alter phenotypic and functional attributes of recipients, reprogramming them into active contributors to angiogenesis, thrombosis, metastasis, and immunosuppression. Exosomes produced by tumors carry cargos that in part mimic contents of parent cells and are of potential interest as noninvasive biomarkers of cancer. Their role in inhibiting the host antitumor responses and in mediating drug resistance is important for cancer therapy. Tumor-derived exosomes may interfere with cancer immunotherapy, but they also could serve as adjuvants and antigenic components of antitumor vaccines. Their biological roles in cancer development or progression as well as cancer therapy suggest that tumor-derived exosomes are critical components of oncogenic transformation.
              Article 0 comments Cited 301 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Gustavo Turecki:
                ORCID: http://orcid.org/0000-0003-4075-2736
                gustavo.turecki@mcgill.ca
                Journal
                Journal ID (nlm-ta): Transl Psychiatry
                Journal ID (iso-abbrev): Transl Psychiatry
                Title: Translational Psychiatry
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2158-3188
                Publication date (Electronic): 28 March 2019
                Publication date PMC-release: 28 March 2019
                Publication date Collection: 2019
                Volume: 9
                Electronic Location Identifier: 122
                Affiliations
                [1 ]ISNI 0000 0004 1936 8649, GRID grid.14709.3b, McGill Group for Suicide Studies, Douglas Mental Health University Institute, , McGill University, ; Montreal, QC Canada
                [2 ]ISNI 0000 0004 1936 8649, GRID grid.14709.3b, Department of Human Genetics, , McGill University, ; Montreal, QC Canada
                [3 ]ISNI 0000 0004 1936 8649, GRID grid.14709.3b, Department of Psychiatry, , McGill University, ; Montreal, QC Canada
                Author information
                http://orcid.org/0000-0003-4075-2736
                Article
                Publisher ID: 459
                DOI: 10.1038/s41398-019-0459-9
                PMC ID: 6438960
                PubMed ID: 30923321
                SO-VID: dd171703-673f-41db-bffe-47bbc5ed9d83
                Copyright © © The Author(s) 2019
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 15 November 2018
                Date revision received : 13 February 2019
                Date accepted : 12 March 2019
                Funding
                Funded by: FundRef https://doi.org/10.13039/501100000024, Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de Recherche en Santé du Canada);
                Award ID: FDN148374
                Award ID: EGM141899
                Award Recipient :
                Categories
                Subject: Review Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2019

                ScienceOpen disciplines: Clinical Psychology & Psychiatry
                Data availability:
                ScienceOpen disciplines: Clinical Psychology & Psychiatry

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