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

First Author  Yuyama K Year  2015
Journal  FEBS Lett Volume  589
Issue  1 Pages  84-8
PubMed ID  25436414 Mgi Jnum  J:216962
Mgi Id  MGI:5610082 Doi  10.1016/j.febslet.2014.11.027
Citation  Yuyama K, et al. (2015) A potential function for neuronal exosomes: Sequestering intracerebral amyloid-beta peptide. FEBS Lett 589(1):84-8
abstractText  Elevated amyloid-beta peptide (Abeta) in brain contributes to Alzheimer's disease (AD) pathogenesis. We demonstrated the presence of exosome-associated Abeta in the cerebrospinal fluid (CSF) of cynomolgus monkeys and APP transgenic mice. The levels of exosome-associated Abeta notably decreased in the CSF of aging animals. We also determined that neuronal exosomes, but not glial exosomes, had abundant glycosphingolipids and could capture Abeta. Infusion of neuronal exosomes into brains of APP transgenic mice decreased Abeta and amyloid depositions, similarly to what reported previously on neuroblastoma-derived exosomes. These findings highlight the role of neuronal exosomes in Abeta clearance, and suggest that their downregulation might relate to Abeta accumulation and, ultimately, the development of AD pathology.
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