Prion-like Mechanisms in the Pathogenesis of Tauopathies and Synucleinopathies

  • Michel Goedert
  • Ben Falcon
  • Florence Clavaguera
  • Markus Tolnay
Genetics (V Bonifati, Section Editor)

DOI: 10.1007/s11910-014-0495-z

Cite this article as:
Goedert, M., Falcon, B., Clavaguera, F. et al. Curr Neurol Neurosci Rep (2014) 14: 495. doi:10.1007/s11910-014-0495-z
Part of the following topical collections:
  1. Topical Collection on Genetics

Abstract

Neurodegenerative diseases, including Alzheimer’s disease and Parkinson’s disease, are characterized by the abnormal aggregation of a small number of intracellular proteins, with tau and α-synuclein being the most commonly affected. Until recently, the events leading to aggregate formation were believed to be entirely cell-autonomous, with protein misfolding occurring independently in many cells. It is now believed that protein aggregates form in a small number of brain cells, from which they propagate intercellularly through templated recruitment, reminiscent of the mechanisms by which prions spread through the nervous system.

Keywords

Tau protein Alpha-synuclein Prions Neurodegeneration 

Copyright information

© Springer Science+Business Media New York 2014

Authors and Affiliations

  • Michel Goedert
    • 1
  • Ben Falcon
    • 1
  • Florence Clavaguera
    • 2
  • Markus Tolnay
    • 2
  1. 1.MRC Laboratory of Molecular BiologyCambridgeUK
  2. 2.Department of NeuropathologyInstitute of PathologyBaselSwitzerland

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