Journal
FRONTIERS IN NEUROSCIENCE
Volume 11, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fnins.2017.00229
Keywords
exosome; Alzheimer's disease; amyloid-beta; glycosphingolipid; microglia
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Funding
- Grants-in-Aid for Scientific Research [26440041] Funding Source: KAKEN
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The intracerebral level of the aggregation-prone peptide, amyloid-beta (A beta), is constantly maintained by multiple clearance mechanisms, including several degradation enzymes, and brain efflux. Disruption of the clearance machinery and the resultant A beta accumulation gives rise to neurotoxic assemblies, leading to the pathogenesis of Alzheimer's disease (AD). In addition to the classic mechanisms of A beta clearance, the protein may be processed by secreted vesicles, although this possibility has not been extensively investigated. We showed that neuronal exosomes, a subtype of extracellular nanovesicles, enwrap, or trap A beta and transport it into microglia for degradation. Here, we review A beta sequestration and elimination by exosomes, and discuss how this clearance machinery might contribute to AD pathogenesis and how it might be exploited for effective AD therapy.
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