This is no surprise to any of us who have been treating our autistic kids for mercury toxicity and oxidative stress for years, but the big surprise in this study is in the credits.
The shocker is that this study is brought to you by Autism Speaks.
IMHO Autism Speaks has finally said something worth saying.
So... will we see this article in the press? Will the AAP recognize it and start looking at Vit. E as a helper for their patients with autism? Will CDC start taking another look at vaccines? Will Autism Speaks start coming around now that their own studies are implicating mercury as a factor in the development of autism?
Or will they all continue to proffer the lie that there is no convincing evidence linking vaccines to autism, while ignoring all the studies that are piling up on the hard drives of parents across the country?
American Journal of Biochemistry and Biotechnology 4 (2): 218-225, 2008
© 2008 Science Publications
Corresponding Author: George C. Wagner, Psychology, Busch Campus, Rutgers University, New Brunswick, NJ 08854
Tel: 732-445-4660 Fax: 732-445-2263
Evidence of Oxidative Stress in Autism Derived from Animal Models
1Xue Ming, 2Michelle A. Cheh and 2Carrie L. Yochum,
3Alycia K. Halladay and 2George C. Wagner
1Pediatric Neuroscience, UMDNJ, Newark, NJ
2Psychology, Rutgers University, New Brunswick, NJ
3Autism Speaks, Princeton, NJ
Abstract: Autism is a pervasive neurodevelopmental disorder that leads to deficits in social interaction, communication and restricted, repetitive motor movements. Autism is a highly heritable disorder, however, there is mounting evidence to suggest that toxicant-induced oxidative stress may play a role. The focus of this article will be to review our animal model of autism and discuss our evidence that oxidative stress may be a common underlying mechanism of neurodevelopmental damage. We have shown that mice exposed to either methylmercury (MeHg) or valproic acid (VPA) in early postnatal life display aberrant social, cognitive and motor behavior. Interestingly, early exposure to both compounds has been clinically implicated in the development of autism. We recently found that Trolox, a water-soluble vitamin E derivative, is capable of attenuating a number of neurobehavioral alterations observed in mice postnatally exposed to MeHg. In addition, a number of other investigators have shown that oxidative stress plays a role in neural injury following MeHg exposure both in vitro and in vivo. New data presented here will show that VPA-induced neurobehavioral deficits are attenuated by vitamin E as well and that the level of glial fibrillary acidic protein (GFAP), a marker of astrocytic neural injury, is altered following VPA exposure. Collectively, these data indicate that vitamin E and its derivative are capable of protecting against neurobehavioral deficits induced by both MeHg and VPA. This antioxidant protection suggests that oxidative stress may be a common mechanism of injury leading to aberrant behavior in both our animal model as well as in the human disease state.