Journal
MOLECULAR NEUROBIOLOGY
Volume 47, Issue 2, Pages 561-574Publisher
SPRINGER
DOI: 10.1007/s12035-012-8267-8
Keywords
alpha-Synuclein; Neuroinflammation; Prion-like; Parkinson's disease; Synucleinopathies; Dual-hit hypothesis; Proteinopathy
Categories
Funding
- European Research Council
- Swedish Research Council
- Human Frontier Science Program
- Parkinson Foundation in Sweden
- ERA-Net NEURON-MIPROTRAN
- Roche Postdoctoral Fellowship
Ask authors/readers for more resources
Parkinson's disease patients exhibit progressive spreading of aggregated alpha-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 alpha-synuclein pathology. Little is known about factors that might affect the prion-like behavior of misfolded alpha-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 alpha-synuclein, which might set in motion events that lead to Parkinson's disease neuropathology. We propose that neuroinflammation promotes the prion-like behavior of alpha-synuclein and that novel anti-inflammatory therapies targeting this mechanism could slow disease progression.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available