1. Blaylock RL, Strunecka A. {{Immune-glutamatergic dysfunction as a central mechanism of the autism spectrum disorders}}. {Curr Med Chem};2009;16(2):157-170.
Despite the great number of observations being made concerning cellular and the molecular dysfunctions associated with autism spectrum disorders (ASD), the basic central mechanism of these disorders has not been proposed in the major scientific literature. Our review brings evidence that most heterogeneous symptoms of ASD have a common set of events closely connected with dysregulation of glutamatergic neurotransmission in the brain with enhancement of excitatory receptor function by pro-inflammatory immune cytokines as the underlying mechanism. We suggest that environmental and dietary excitotoxins, mercury, fluoride, and aluminum can exacerbate the pathological and clinical problems by worsening excitotoxicity and by microglial priming. In addition, each has effects on cell signaling that can affect neurodevelopment and neuronal function. Our hypothesis opens the door to a number of new treatment modes, including the nutritional factors that naturally reduce excitotoxicity and brain inflammation.
2. Hadjikhani N, Joseph RM, Manoach DS, Naik P, Snyder J, Dominick K, Hoge R, Van den Stock J, Tager Flusberg H, de Gelder B. {{Body expressions of emotion do not trigger fear contagion in autism spectrum disorder}}. {Soc Cogn Affect Neurosci};2009 (Mar);4(1):70-78.
Although there is evidence of emotion perception deficits in autism spectrum disorder (ASD), research on this topic has been mostly confined to perception of emotions in faces. Using behavioral measures and 3T functional magnetic resonance imaging (fMRI), we examined whether such deficits extend to the perception of bodily expressed emotions. We found that individuals with ASD, in contrast to neurotypical (NT) individuals, did not exhibit a differential pattern of brain activation to bodies expressing fear as compared with emotionally neutral bodies. ASD and NT individuals showed similar patterns of activation in response to bodies engaged in emotionally neutral actions, with the exception of decreased activation in the inferior frontal cortex and the anterior insula in ASD. We discuss these findings in relation to possible abnormalities in a network of cortical and subcortical mechanisms involved in social orienting and emotion contagion. Our data suggest that emotion perception deficits in ASD may be due to compromised processing of the emotional component of observed actions.
3. Li X, Chauhan A, Sheikh AM, Patil S, Chauhan V, Li XM, Ji L, Brown T, Malik M. {{Elevated immune response in the brain of autistic patients}}. {J Neuroimmunol};2009 (Feb 15);207(1-2):111-116.
This study determined immune activities in the brain of ASD patients and matched normal subjects by examining cytokines in the brain tissue. Our results showed that proinflammatory cytokines (TNF-alpha, IL-6 and GM-CSF), Th1 cytokine (IFN-gamma) and chemokine (IL-8) were significantly increased in the brains of ASD patients compared with the controls. However the Th2 cytokines (IL-4, IL-5 and IL-10) showed no significant difference. The Th1/Th2 ratio was also significantly increased in ASD patients. Conclusion: ASD patients displayed an increased innate and adaptive immune response through the Th1 pathway, suggesting that localized brain inflammation and autoimmune disorder may be involved in the pathogenesis of ASD.
