Volume 8 Supplement 1

Molecular Neurodegeneration: Basic biology and disease pathways

Open Access

Prion-like aspects of cerebral amyloidosis

  • Mathias Jucker1,
  • Lan Ye1 and
  • Sarah Fritschi1
Molecular Neurodegeneration20138(Suppl 1):O21

https://doi.org/10.1186/1750-1326-8-S1-O21

Published: 13 September 2013

The commonality of many neurodegenerative disorders is the predictable temporal occurrence and progression of specific aggregated proteins in the brain. The hallmark proteopathy is Alzheimer’s disease in which aggregated amyloid-β peptide (Aβ) is deposited in the brain parenchyma as amyloid plaques. Multiple evidence suggests that β-amyloidosis is induced by aggregated Aβ which can spread within and among brain regions and act as corruptive templates (seeds) that induce a chain-reaction of Aβ misfolding and aggregation. The insight that the prion paradigm may also apply to cerebral β-amyloidosis and other proteopathies suggests new avenues in search of biomarkers and novel therapeutic strategies.

Authors’ Affiliations

(1)
Department of Cellular Neurology, Hertie Institute for Clinical Brain, Research, University of Tübingen, and German Center for Neurodegenerative Diseases (DZNE)

Copyright

© Jucker et al; licensee BioMed Central Ltd. 2013

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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