Exosomes neutralize synaptic-plasticity-disrupting activity of Aβ assemblies in vivo
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Author
An, Kyongman
Klyubin, Igor
Kim, Youngkyu
Jung, Jung Hoon
O’Dowd, Sean T
Lynch, Timothy
Finan, Gina M
Park, Joon Won
Kim, Tae-Wan
Rowan, Michael J
Kim, Joung-Hun
Note: Order does not necessarily reflect citation order of authors.
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https://doi.org/10.1186/1756-6606-6-47Metadata
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An, K., I. Klyubin, Y. Kim, J. H. Jung, A. J. Mably, S. T. O’Dowd, T. Lynch, et al. 2013. “Exosomes neutralize synaptic-plasticity-disrupting activity of Aβ assemblies in vivo.” Molecular Brain 6 (1): 47. doi:10.1186/1756-6606-6-47. http://dx.doi.org/10.1186/1756-6606-6-47.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 PrPC 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.Other Sources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4222117/pdf/Terms of Use
This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAACitable link to this page
http://nrs.harvard.edu/urn-3:HUL.InstRepos:13454718
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