Journal
ACTA NEUROPATHOLOGICA
Volume 136, Issue 1, Pages 41-56Publisher
SPRINGER
DOI: 10.1007/s00401-018-1868-1
Keywords
Alzheimer's disease; Exosomes; Oligomers; Beta-amyloid; Human; Prion-like; Propagation
Categories
Funding
- Swedish Research Council [MH: 523-2013-2735]
- Swedish Alzheimer foundation
- Swedish Brain Foundation
- Hans-Gabriel and Alice Trolle-Wachtmeister Foundation for Medical Research
- Konung Gustaf V:s och Drottning Victorias Frimurarestiftelse
- Marianne and Marcus Wallenberg Foundation
- Swedish Fund for Research without Animal Experiments
- Swedish Dementia Foundation
- Linkoping University Neurobiology Centre
- County Council of Ostergotland
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The gradual deterioration of cognitive functions in Alzheimer's disease is paralleled by a hierarchical progression of amyloid-beta and tau brain pathology. Recent findings indicate that toxic oligomers of amyloid-beta may cause propagation of pathology in a prion-like manner, although the underlying mechanisms are incompletely understood. Here we show that small extracellular vesicles, exosomes, from Alzheimer patients' brains contain increased levels of amyloid-beta oligomers and can act as vehicles for the neuron-to-neuron transfer of such toxic species in recipient neurons in culture. Moreover, blocking the formation, secretion or uptake of exosomes was found to reduce both the spread of oligomers and the related toxicity. Taken together, our results imply that exosomes are centrally involved in Alzheimer's disease and that they could serve as targets for development of new diagnostic and therapeutic principles.
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