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Alzheimers disease pathology propagation by exosomes containing toxic amyloid-beta oligomers
Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Clinical pathology.
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2018 (English)In: Acta Neuropathologica, ISSN 0001-6322, E-ISSN 1432-0533, Vol. 136, no 1, p. 41-56Article in journal (Refereed) Published
Abstract [en]

The gradual deterioration of cognitive functions in Alzheimers 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 Alzheimers disease and that they could serve as targets for development of new diagnostic and therapeutic principles.

Place, publisher, year, edition, pages
SPRINGER , 2018. Vol. 136, no 1, p. 41-56
Keywords [en]
Alzheimers disease; Exosomes; Oligomers; Beta-amyloid; Human; Prion-like; Propagation
National Category
Neurosciences
Identifiers
URN: urn:nbn:se:liu:diva-149701DOI: 10.1007/s00401-018-1868-1ISI: 000435940000003PubMedID: 29934873OAI: oai:DiVA.org:liu-149701DiVA, id: diva2:1233569
Note

Funding Agencies|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

Available from: 2018-07-18 Created: 2018-07-18 Last updated: 2019-04-24

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