Prion-like mechanisms in neurodegenerative diseases

Nat Rev Neurosci. 2010 Mar;11(3):155-9. doi: 10.1038/nrn2786. Epub 2009 Dec 23.


Many non-infectious neurodegenerative diseases are associated with the accumulation of fibrillar proteins. These diseases all exhibit features that are reminiscent of those of prionopathies, including phenotypic diversity and the propagation of pathology. Furthermore, emerging studies of amyloid-beta, alpha-synuclein and tau--proteins implicated in common neurodegenerative diseases--suggest that they share key biophysical and biochemical characteristics with prions. Propagation of protein misfolding in these diseases may therefore occur through mechanisms similar to those that underlie prion pathogenesis. If this hypothesis is verified in vivo, it will suggest new therapeutic strategies to block propagation of protein misfolding throughout the brain.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Amyloid beta-Peptides / metabolism
  • Brain / metabolism*
  • Brain / pathology
  • Disease Progression
  • Humans
  • Neurodegenerative Diseases / metabolism*
  • Neurodegenerative Diseases / pathology
  • Prions / metabolism*
  • Protein Conformation
  • alpha-Synuclein / metabolism
  • tau Proteins / metabolism


  • Amyloid beta-Peptides
  • Prions
  • alpha-Synuclein
  • tau Proteins