Microglia, major player in the brain inflammation: Their roles in the pathogenesis of Parkinson's disease

Yoon Seong Kim, Tong H. Joh

Research output: Contribution to journalReview articlepeer-review

533 Scopus citations


Inflammation, a self-defensive reaction against various pathogenic stimuli, may become harmful self-damaging process. Increasing evidence has linked chronic inflammation to a number of neurodegenerative disorders including Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis. In the central nervous system, microglia, the resident innate immune cells play major role in the inflammatory process. Although they form the first line of defense for the neural parenchyma, uncontrolled activation of microglia may directly toxic to neurons by releasing various substances such as inflammatory cytokines (IL-1β, TNF-α, IL-6), NO, PGE2, and superoxide. Moreover, our recent study demonstrated that activated microglia phagocytose not only damaged cell debris but also neighboring intact cells. It further supports their active participation in self-perpetuating neuronal damaging cycles. In the following review, we discuss microglial responses to damaging neurons, known activators released from injured neurons and how microglia cause neuronal degeneration. In the last part, microglial activation and their role in PD are discussed in depth.

Original languageEnglish (US)
Pages (from-to)333-347
Number of pages15
JournalExperimental and Molecular Medicine
Issue number4
StatePublished - Aug 31 2006
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Medicine
  • Molecular Biology
  • Clinical Biochemistry


  • Inflammation
  • Microglia
  • Neurodegenerative diseases
  • Parkinson's disease
  • Phagocytosis
  • Stromelysin 1
  • Superoxides


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