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Curr Neurol Neurosci Rep. 2014 Nov;14(11):495. doi: 10.1007/s11910-014-0495-z.

Prion-like mechanisms in the pathogenesis of tauopathies and synucleinopathies.

Author information

1
MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge, CB2 0QH, UK, mg@mrc-lmb.cam.ac.uk.

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.

PMID:
25218483
DOI:
10.1007/s11910-014-0495-z
[Indexed for MEDLINE]

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