Inflammation and α-synuclein's prion-like behavior in Parkinson's disease--is there a link?

Abstract

Parkinson's disease patients exhibit progressive spreading of aggregated α-synuclein in the nervous system. This slow process follows a specific pattern in an inflamed tissue environment. Recent research suggests that prion-like mechanisms contribute to the propagation of α-synuclein pathology. Little is known about factors that might affect the prion-like behavior of misfolded α-synuclein. In this review, we suggest that neuroinflammation plays an important role. We discuss causes of inflammation in the olfactory bulb and gastrointestinal tract and how this may promote the initial misfolding and aggregation of α-synuclein, which might set in motion events that lead to Parkinson's disease neuropathology. We propose that neuroinflammation promotes the prion-like behavior of α-synuclein and that novel anti-inflammatory therapies targeting this mechanism could slow disease progression.

• Authors: Carla M Lema Tomé, Trevor Tyson, Nolwen L Rey, Stefan Grathwohl, Markus Britschgi, Patrik Brundin
• Journal: Molecular neurobiology (Mol Neurobiol) Vol. 47 Issue 2 Pg. 561-74 (Apr 2013) ISSN: 1559-1182 [Electronic] United States
• PMID: 22544647 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Anti-Inflammatory Agents, Non-Steroidal
• Prions
• alpha-Synuclein

Topics

• Animals
• Anti-Inflammatory Agents, Non-Steroidal (pharmacology, therapeutic use)
• Cell Communication (drug effects, physiology)
• Humans
• Inflammation (drug therapy, metabolism, pathology)
• Olfactory Bulb (drug effects, metabolism, pathology)
• Parkinson Disease (drug therapy, metabolism, pathology)
• Prions (drug effects, metabolism)
• alpha-Synuclein (metabolism)