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

Hdl Handle:
http://hdl.handle.net/10147/315475
Title:
Exosomes neutralize synaptic-plasticity-disrupting activity of Aβ assemblies in vivo
Authors:
An, Kyongman; Klyubin, Igor; Kim, Youngkyu; Jung, Jung H; Mably, Alexandra J; O’Dowd, Sean T; Lynch, Timothy; Kanmert, Daniel; Lemere, Cynthia A; Finan, Gina M; Park, Joon W; Kim, Tae-Wan; Walsh, Dominic M; Rowan, Michael J; Kim, Joung-Hun
Citation:
Molecular brain. 2013 Nov 13;6(1):47
Journal:
Molecular brain
Issue Date:
13-Nov-2013
URI:
http://dx.doi.org/10.1186/1756-6606-6-47; http://hdl.handle.net/10147/315475
Abstract:
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.
Item Type:
Article
Language:
en
Keywords:
NEOROLOGICAL DISEASE AND DISORDER
Local subject classification:
MOLECULAR BIOLOGY; BRAIN

Full metadata record

DC FieldValue Language
dc.contributor.authorAn, Kyongmanen_GB
dc.contributor.authorKlyubin, Igoren_GB
dc.contributor.authorKim, Youngkyuen_GB
dc.contributor.authorJung, Jung Hen_GB
dc.contributor.authorMably, Alexandra Jen_GB
dc.contributor.authorO’Dowd, Sean Ten_GB
dc.contributor.authorLynch, Timothyen_GB
dc.contributor.authorKanmert, Danielen_GB
dc.contributor.authorLemere, Cynthia Aen_GB
dc.contributor.authorFinan, Gina Men_GB
dc.contributor.authorPark, Joon Wen_GB
dc.contributor.authorKim, Tae-Wanen_GB
dc.contributor.authorWalsh, Dominic Men_GB
dc.contributor.authorRowan, Michael Jen_GB
dc.contributor.authorKim, Joung-Hunen_GB
dc.date.accessioned2014-04-07T11:24:50Z-
dc.date.available2014-04-07T11:24:50Z-
dc.date.issued2013-11-13-
dc.identifier.citationMolecular brain. 2013 Nov 13;6(1):47en_GB
dc.identifier.urihttp://dx.doi.org/10.1186/1756-6606-6-47-
dc.identifier.urihttp://hdl.handle.net/10147/315475-
dc.description.abstractAbstract 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.-
dc.language.isoenen
dc.subjectNEOROLOGICAL DISEASE AND DISORDERen_GB
dc.subject.otherMOLECULAR BIOLOGYen_GB
dc.subject.otherBRAINen_GB
dc.titleExosomes neutralize synaptic-plasticity-disrupting activity of Aβ assemblies in vivoen_GB
dc.typeArticleen
dc.identifier.journalMolecular brainen_GB
dc.language.rfc3066en-
dc.rights.holderKyongman An et al.; licensee BioMed Central Ltd.-
dc.description.statusPeer Reviewed-
dc.date.updated2014-04-05T11:16:18Z-
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