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      Exosomes neutralize synaptic-plasticity-disrupting activity of Aβ assemblies in vivo

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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

          Background

          Exosomes, small extracellular vesicles of endosomal origin, have been suggested to be involved in both the metabolism and aggregation of Alzheimer’s disease (AD)-associated amyloid β-protein (Aβ). Despite their ubiquitous presence and the inclusion of components which can potentially interact with Aβ, the role of exosomes in regulating synaptic dysfunction induced by Aβ has not been explored.

          Results

          We here provide in vivo evidence that exosomes derived from N2a cells or human cerebrospinal fluid can abrogate the synaptic-plasticity-disrupting activity of both synthetic and AD brain-derived Aβ. Mechanistically, this effect involves sequestration of synaptotoxic Aβ assemblies by exosomal surface proteins such as PrP C rather than Aβ proteolysis.

          Conclusions

          These data suggest that exosomes can counteract the inhibitory action of Aβ, which contributes to perpetual capability for synaptic plasticity.

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          Most cited references 53

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          The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics.

           D. Selkoe,  John Hardy (2002)
          It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer's disease (AD) may be caused by deposition of amyloid beta-peptide (Abeta) in plaques in brain tissue. According to the amyloid hypothesis, accumulation of Abeta in the brain is the primary influence driving AD pathogenesis. The rest of the disease process, including formation of neurofibrillary tangles containing tau protein, is proposed to result from an imbalance between Abeta production and Abeta clearance.
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            • Abstract: not found
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            Exosomes: composition, biogenesis and function.

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              • Article: not found

              Alzheimer's disease is a synaptic failure.

               D. Selkoe (2002)
              In its earliest clinical phase, Alzheimer's disease characteristically produces a remarkably pure impairment of memory. Mounting evidence suggests that this syndrome begins with subtle alterations of hippocampal synaptic efficacy prior to frank neuronal degeneration, and that the synaptic dysfunction is caused by diffusible oligomeric assemblies of the amyloid beta protein.
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                Author and article information

                Contributors
                Journal
                Mol Brain
                Mol Brain
                Molecular Brain
                BioMed Central
                1756-6606
                2013
                13 November 2013
                : 6
                : 47
                Affiliations
                [1 ]Department of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang, Gyungbuk 790-784, Korea
                [2 ]Department of Pharmacology and Therapeutics, and Institute of Neuroscience, Biotechnology Building, Trinity College, Dublin 2, Ireland
                [3 ]School of Interdisciplinary Bioscience and Bioengineering, Pohang University of Science and Technology (POSTECH), Pohang, Gyungbuk 790-784, Korea
                [4 ]Laboratory for Neurodegenerative Research, Center for Neurologic Diseases, Brigham & Women’s Hospital, Harvard Institute of Medicine, 77 Avenue Louis Pasteur, Boston, MA 02115, USA
                [5 ]Laboratory for Neurodegenerative Research, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin 4, Ireland
                [6 ]Dublin Neurological Institute at the Mater Misericordiae University Hospital, 57 Eccles Street, Dublin 7, Ireland
                [7 ]Department of Pathology and Cell Biology, Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University, New York, NY 10032, USA
                Article
                1756-6606-6-47
                10.1186/1756-6606-6-47
                4222117
                24284042
                Copyright © 2013 An et al.; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                Categories
                Research

                Neurosciences

                alzheimer’s disease, , exosomes, synaptic plasticity, prpc

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