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Autism, Mitochondria and Polybrominated Diphenyl Ether Exposure
1University of California, Department of Molecular Biosciences, 1089 Veterinary Medicine Dr., 3009 VetMed3B, Davis, CA 95616, USA. cgiulivi@ucdavis.edu.
CNS & Neurological Disorders Drug Targets
|April 14, 2016
Summary
Polybrominated diphenyl ethers (PBDEs) exposure during development may increase autism risk by causing mitochondrial dysfunction. This dysfunction, coupled with antioxidant issues, heightens a child's susceptibility to autism spectrum disorder (ASD).
Area of Science:
- Environmental Health
- Neurodevelopmental Disorders
- Toxicology
Background:
- Autism spectrum disorders (ASD) affect over 1 in 68 children in the US by age 8.
- The etiology of ASD is multifactorial, involving both genetic and environmental factors.
- Limited progress has been made in understanding the specific causes of ASD.
Purpose of the Study:
- To investigate the potential link between polybrominated diphenyl ethers (PBDE) exposure and autism risk.
- To explore the role of mitochondrial dysfunction as a mediator in this relationship.
- To understand how environmental factors like PBDEs may contribute to ASD.
Main Methods:
- This is a review article, synthesizing existing research.
- The review examines the environmental abundance and human exposure levels of PBDEs.
- It analyzes the known effects of PBDEs on neuronal development, synaptic plasticity, and mitochondria.
Main Results:
- PBDEs are environmentally abundant and humans are exposed to them.
- PBDEs exhibit activity relevant to neuronal development and mitochondrial function.
- PBDEs bioaccumulate within mitochondria, suggesting a direct impact on cellular energy production.
Conclusions:
- Perinatal PBDE exposure may contribute to ASD etiology and morbidity.
- PBDEs can induce or exacerbate mitochondrial dysfunction during child development.
- This mitochondrial dysfunction, alongside a compromised antioxidant response, increases autism susceptibility.

