Autism is a behaviorally-defined neurodevelopmental disorder that is difficult to diagnose, treat, and study due to its unknown etiology, widely varying symptoms, and lack of an identified neuropathology. In contrast, Parkinson's disease is a neurodegenerative disease of unknown etiology that is well defined both behaviorally and neuropathologically. While clinically these two disorders appear to have little in common, we would like to present the hypothesis that their respective etiologies may share similar features. Both autism and Parkinson's disease are thought to be the result of interactions between environmental insult, genetic polymorphisms, and age. In addition, since no particular environmental toxicant has been identified as causal for either condition, we propose that any of a number of possible environmental toxicants interact with the individual's genetic sensitivity to cause the underlying neuronal damage. We suggest that while low levels of exposure to any of these individual toxicants may be well-tolerated by most individuals during early development, various combinations of the toxicants may exert a cumulative, deleterious effect. Likewise, although several genes have been linked to autism and Parkinson's disease, respectively, no single gene has been identified that can account for a majority of cases for either. Therefore, various combinations of genetic alterations predispose individuals to their respective disorders but it remains the case that the environmental exposure(s) must occur during critical periods of development for the eventual disease manifestation. The objective of this review is to provide examples from animal models that the etiologies of autism and Parkinson's disease have common features of toxicant-induced oxidative stress together with genetic deficiencies in the ability to manage reactive oxygen species and, furthermore, that therapeutic intervention using antioxidants delivered at the time of toxicant exposure may be beneficial for both.
All Science Journal Classification (ASJC) codes
- Physiology (medical)
- Animal models
- Parkinson's disease
- Reactive oxygen species