[HTML][HTML] Exosomes neutralize synaptic-plasticity-disrupting activity of Aβ assemblies in vivo
Molecular brain, 2013•Springer
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 …
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 …
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.
Springer