Parkinson's disease, proteins, and prions: Milestones

C. Warren Olanow, K. Mcnaught

Research output: Contribution to journalReview articlepeer-review

41 Scopus citations

Abstract

Parkinson's disease (PD) is characterized by protein accumulation in the form of Lewy bodies and neurites. It is thus reasonable to consider that alterations in protein handling in the form of increased production, impaired clearance, or both might be central to the etiopathogenesis of the disease. Increasing genetic, laboratory and pathologic evidence has accumulated over the past 25 years supporting this hypothesis. A vicious cycle could develop in which increased protein accumulation from any cause could lead to interference with lysosomal and proteasomal clearance mechanisms causing further protein accumulation. Eventually, protein accumulation could overwhelm the cell's defenses and lead to the formation of toxic oligomers and amyloid-based inclusions such as Lewy bodies, disruption of critical cell processes, and ultimately neurodegeneration. More recent findings of Lewy pathology in implanted embryonic dopamine neurons in PD patients raises the intriguing possibility that PD might be a prion disorder. These concepts suggests new targets and novel candidate therapies that might be neuroprotective for PD.

Original languageEnglish
Pages (from-to)1056-1071
Number of pages16
JournalMovement Disorders
Volume26
Issue number6
DOIs
StatePublished - May 2011

Keywords

  • PD
  • Prions
  • Proteins

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