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Autism Studies and Related Medical Conditions, January 2009 - TACA

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5 - <strong>Autism</strong> <strong>and</strong> Oxidative Stress (70 citations):<br />

Abbott, L. C. <strong>and</strong> S. S. Nahm (2004). "Neuronal nitric oxide synthase expression in<br />

cerebellar mutant mice." Cerebellum 3(3): 141-51.<br />

Nitric oxide (NO) is a diffusible, multifunctional signaling molecule found in many<br />

areas of the brain. NO signaling is involved in a wide array of neurophysiological<br />

functions including synaptogenesis, modulation of neurotransmitter release,<br />

synaptic plasticity, central nervous system blood flow <strong>and</strong> cell death. NO<br />

synthase (NOS) activity regulates the production of NO <strong>and</strong> the cerebellum<br />

expresses high levels of nitric oxide synthase (NOS) in granule, stellate <strong>and</strong><br />

basket cells. Cerebellar mutant mice provide excellent opportunities to study<br />

changes of NO/NOS concentrations <strong>and</strong> activities to gain a greater underst<strong>and</strong>ing<br />

of the roles of NO <strong>and</strong> NOS in cerebellar function. Here, we have reviewed the<br />

current underst<strong>and</strong>ing of the functional roles of NO <strong>and</strong> NOS in the cerebellum<br />

<strong>and</strong> present NO/NOS activities that have been described in various cerebellar<br />

mutant mice <strong>and</strong> NOS knockout mice. NO appears to exert neuroprotective<br />

effects at low to moderate concentrations, whereas NO becomes neurotoxic as<br />

the concentration increases. Excessive NO production can cause oxidative stress<br />

to neurons, ultimately impairing neuronal function <strong>and</strong> result in neuronal cell<br />

death. Based on their genetics <strong>and</strong> cerebellar histopathology, some of cerebellar<br />

mutant mice display similarities with human neurological conditions <strong>and</strong> may<br />

prove to be valuable models to study several human neurological disorders, such<br />

as autism <strong>and</strong> schizophrenia.<br />

Amminger, G. P., G. E. Berger, et al. (2007). "Omega-3 fatty acids supplementation in<br />

children with autism: a double-blind r<strong>and</strong>omized, placebo-controlled pilot study." Biol<br />

Psychiatry 61(4): 551-3.<br />

BACKGROUND: There is increasing evidence that fatty acid deficiencies or<br />

imbalances may contribute to childhood neurodevelopmental disorders.<br />

METHODS: We conducted a r<strong>and</strong>omized, double-blind, placebo-controlled 6-<br />

week pilot trial investigating the effects of 1.5 g/d of omega-3 fatty acids (.84<br />

g/d eicosapentaenoic acid, .7 g/d docosahexaenoic acid) supplementation in 13<br />

children (aged 5 to 17 years) with autistic disorders accompanied by severe<br />

tantrums, aggression, or self-injurious behavior. The outcome measure was the<br />

Aberrant Behavior Checklist (ABC) at 6 weeks. RESULTS: We observed an<br />

advantage of omega-3 fatty acids compared with placebo for hyperactivity <strong>and</strong><br />

stereotypy, each with a large effect size. Repeated-measures ANOVA indicated a<br />

trend toward superiority of omega-3 fatty acids over placebo for hyperactivity.<br />

No clinically relevant adverse effects were elicited in either group.<br />

CONCLUSIONS: The results of this study provide preliminary evidence that<br />

omega-3 fatty acids may be an effective treatment for children with autism.<br />

<strong>Autism</strong> <strong>Studies</strong> & <strong>Related</strong> <strong>Medical</strong> <strong>Conditions</strong> – <strong>TACA</strong> © Page 70

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