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FEBS Lett. 2015 Jan 2;589(1):84-8. doi: 10.1016/j.febslet.2014.11.027. Epub 2014 Nov 29.

A potential function for neuronal exosomes: sequestering intracerebral amyloid-β peptide.

Author information

1
Laboratory of Biomembrane and Biofunctional Chemistry, Graduate School of Advanced Life Science, and Frontier Research Center for Post-Genome Science and Technology, Hokkaido University, Sapporo, Japan. Electronic address: kyuyama@pharm.hokudai.ac.jp.
2
Laboratory of Biomembrane and Biofunctional Chemistry, Graduate School of Advanced Life Science, and Frontier Research Center for Post-Genome Science and Technology, Hokkaido University, Sapporo, Japan.
3
Laboratory of Biomembrane and Biofunctional Chemistry, Graduate School of Advanced Life Science, and Frontier Research Center for Post-Genome Science and Technology, Hokkaido University, Sapporo, Japan; Division of Molecular Interaction, Institute for Genetic Medicine, Graduate School of Life Science, Hokkaido University, Sapporo, Japan.
4
Section of Cell Biology and Pathology, Department of Alzheimer's Disease Research, Center for Development of Advanced Medicine for Dementia, National Center for Geriatrics and Gerontology, Obu, Japan.
5
Department of Cellular and Molecular Biology, Graduate School of Biomedical Science, Hiroshima University, Hiroshima, Japan.
6
Laboratory of Medical and Functional Glycomics, Graduate School of Advanced Life Science, and Frontier Research Center for Post-Genome Science and Technology, Hokkaido University, Sapporo, Japan.

Abstract

Elevated amyloid-β peptide (Aβ) in brain contributes to Alzheimer's disease (AD) pathogenesis. We demonstrated the presence of exosome-associated Aβ in the cerebrospinal fluid (CSF) of cynomolgus monkeys and APP transgenic mice. The levels of exosome-associated Aβ notably decreased in the CSF of aging animals. We also determined that neuronal exosomes, but not glial exosomes, had abundant glycosphingolipids and could capture Aβ. Infusion of neuronal exosomes into brains of APP transgenic mice decreased Aβ and amyloid depositions, similarly to what reported previously on neuroblastoma-derived exosomes. These findings highlight the role of neuronal exosomes in Aβ clearance, and suggest that their downregulation might relate to Aβ accumulation and, ultimately, the development of AD pathology.

KEYWORDS:

APP transgenic mouse; Alzheimer’s disease; Amyloid-β peptide; Cerebrospinal fluid; Cynomolgus monkey; Exosome

PMID:
25436414
DOI:
10.1016/j.febslet.2014.11.027
[Indexed for MEDLINE]
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