Research ArticleParkinson’s Disease

Inflammasome inhibition prevents α-synuclein pathology and dopaminergic neurodegeneration in mice

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Science Translational Medicine  31 Oct 2018:
Vol. 10, Issue 465, eaah4066
DOI: 10.1126/scitranslmed.aah4066

Systemic inflammasome inhibitor for Parkinson’s disease

Brain accumulation of misfolded α-synuclein, progressive loss of dopaminergic neurons, and neuroinflammation are major hallmarks of Parkinson’s disease (PD). Although neuroinflammation has been shown to contribute to the pathophysiology of the disease, the mechanisms mediating the activation of inflammatory signals remain unclear. Gordon and colleagues now show that, in mouse models of PD, α-synuclein aggregates promote inflammasome activation in brain microglia. Oral treatment with an inflammasome inhibitor improved motor performance and reduced neuroinflammation, neurodegeneration, and α-synuclein accumulation in mouse models of α-synuclein–mediated toxicity. The results suggest that systemic delivery of inflammasome inhibitors might have therapeutic effects in PD.

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