The role of chronic inflammation in the etiology of parkinson’s disease

Yuval Nash, Dan Frenkel

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

Abstract

Parkinson’s disease (PD) is a neurodegenerative disease that is characterized by specific pathological features such as the death of dopaminergic neurons and formation of Lewy bodies. Another marker of stress that is found in patients and PD animal models is an increase in inflammation. Different cells are found to be allocated to this process, such as resident brain cells, specifically microglia and astrocytes, and peripheral infiltrated cells such as T cells and monocytes. Those inflammatory cells may secrete different stress factors such as IL-1β and reactive oxygen species that might exacerbate neuronal death. However, there is also evidence that those cells may also secrete neuroprotective factors that may support stressed cells. This review will aim to address the role of those inflammatory cells in the progression of PD.

Original languageEnglish
Title of host publicationMitochondrial Mechanisms of Degeneration and Repair in Parkinson's Disease
PublisherSpringer International Publishing
Pages63-74
Number of pages12
ISBN (Electronic)9783319421391
ISBN (Print)9783319421377
DOIs
StatePublished - 1 Jan 2016

Keywords

  • Inflammation
  • Microglia
  • Parkinson’s disease
  • T cells

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