Prion-like spread of protein aggregates in neurodegeneration.

The Journal of Experimental Medicine
Magdalini Polymenidou, Don W Cleveland

Abstract

Protein misfolding is common to most neurodegenerative diseases, including Alzheimer's and Parkinson's diseases. Recent work using animal models with intracellular α-synuclein and tau inclusions adds decisively to a growing body of evidence that misfolded protein aggregates can induce a self-perpetuating process that leads to amplification and spreading of pathological protein assemblies. When coupled with the progressive nature of neurodegeneration, recognition of such cell-to-cell aggregate spread suggests a unifying mechanism underlying the pathogenesis of these disorders.

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Methods Mentioned

BETA
laser capture microdissection

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