期刊
MOLECULAR NEUROBIOLOGY
卷 47, 期 2, 页码 561-574出版社
SPRINGER
DOI: 10.1007/s12035-012-8267-8
关键词
alpha-Synuclein; Neuroinflammation; Prion-like; Parkinson's disease; Synucleinopathies; Dual-hit hypothesis; Proteinopathy
资金
- European Research Council
- Swedish Research Council
- Human Frontier Science Program
- Parkinson Foundation in Sweden
- ERA-Net NEURON-MIPROTRAN
- Roche Postdoctoral Fellowship
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.
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