Neuroinflammation and oxidative injury in developmental neurotoxicity

Dejan Milatovic, Snjezana Zaja-Milatovic, Mirjana Milosevic Brockett, Richard M. Breyer, Michael Aschner, Thomas J. Montine

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Neuroinflammation is a complex response to brain injury involving the activation of glia, release of inflammatory mediators, such as cytokines and chemokines, and generation of reactive oxygen and nitrogen species. Inflammatory responses in the brain are associated with increased levels of prostaglandins (PGs), particularly PGE2. The PGE2 signaling is mediated by interactions with four distinct G protein-coupled receptors, EP1, EP2, EP3, and EP4, which are differentially expressed on neuronal and glial cells throughout the central nervous system. Elevated PGE2 and inflammatory mediators are also inherent to the aging brain. An increased state of neuroinflammation renders the aged brain more vulnerable to the disruptive effects of both intrinsic and extrinsic factors such as disease, infection, toxicants, or stress. This chapter characterizes processes of neuroinflammation and related oxidative injury and discusses neuroinflammatory changes associated with aging.

Original languageEnglish (US)
Title of host publicationReproductive and Developmental Toxicology
PublisherElsevier
Pages1129-1140
Number of pages12
ISBN (Electronic)9780323897730
ISBN (Print)9780323915601
DOIs
StatePublished - Jan 1 2022

Keywords

  • Developmental neurotoxicity
  • Neuroinflammation
  • Oxidative stress

ASJC Scopus subject areas

  • Medicine(all)

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