期刊
MOLECULAR BRAIN
卷 6, 期 -, 页码 -出版社
BMC
DOI: 10.1186/1756-6606-6-47
关键词
Alzheimer's disease; A beta; Exosomes; Synaptic plasticity; PrPC
资金
- Cure Alzheimer Fund
- Science Foundation Ireland
- Health Research Board of Ireland
- European Union Seventh Framework Programme 528 [MEMOLOAD 201159]
- Korea Healthcare technology R&D Project, Ministry of Health Welfare [A092058-1113-0000300, A111284]
- National Research Foundation of Korea, Republic of Korea [2011-0000835]
- Korea Health Promotion Institute [A111284] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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 beta-protein (A beta). Despite their ubiquitous presence and the inclusion of components which can potentially interact with A beta, the role of exosomes in regulating synaptic dysfunction induced by A beta 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 A beta. Mechanistically, this effect involves sequestration of synaptotoxic A beta assemblies by exosomal surface proteins such as PrPC rather than A beta proteolysis. Conclusions: These data suggest that exosomes can counteract the inhibitory action of A beta, which contributes to perpetual capability for synaptic plasticity.
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