[The association of Parkinson's disease pathogenesis with inflammation]

Recent research on pathogenesis of neurodegenerative diseases has revealed that neuroinflammation derived from glial activation enhances the progression of devastating diseases including Parkinson's disease (PD). Although whether or not PD-onset is triggered by neuroinflammatory mechanisms remains unclear, various experimental evidences mainly using cellular and mice models have suggested that cytokines like IL-1β, TNFα and IL-6, and secreted α-synuclein from the neurons activate the microglias, resulting in the disease exacerbation. Also, levels of serum/plasma cytokines such as IL-1β, TNFα, IL-2 and ApoA1 have been reported to be significantly elevated in patients with PD compared to the controls. In this summary, I will report the present status of PD pathogenesis associated with neuroinflammation based on the latest reports associated with PD molecular mechanism focusing on the neuroinflammation.