Autism, mitochondria and polybrominated diphenyl ether exposure

Sarah Wong, Cecilia R Giulivi

Research output: Contribution to journalArticlepeer-review

9 Scopus citations

Abstract

Background: Autism spectrum disorders (ASD) are a growing concern with more than 1 in every 68 children affected in the United States by age 8. Limited scientific advances have been made regarding the etiology of autism, with general agreement that both genetic and environmental factors contribute to this disorder. Objective: To explore the link between exposure to PBDE, mitochondrial dysfunction and autism risk. Results: Perinatal exposures to PBDEs may contribute to the etiology or morbidity of ASD including mitochondrial dysfunction based on (i) their increased environmental abundance and human exposures, (ii) their activity towards implicated in neuronal development and synaptic plasticity including mitochondria, and (iii) their bioaccumulation in mitochondria. Conclusion: In this review, we propose that PBDE, and possibly other environmental exposures, during child development can induce or compound mitochondrial dysfunction, which in conjunction with a dysregulated antioxidant response, increase a child’s susceptibility of autism.

Original languageEnglish (US)
Pages (from-to)614-623
Number of pages10
JournalCNS and Neurological Disorders - Drug Targets
Volume15
Issue number5
StatePublished - May 1 2016

Keywords

  • Antioxidant response
  • Autism risk
  • Mitochondrial dysfunction
  • Neuronal development
  • Oxidative stress
  • PBDE exposure

ASJC Scopus subject areas

  • Neuroscience(all)
  • Pharmacology

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