Autism spectrum disorder (ASD) is a social, sensory and developmental condition that affects one in 59 children and specifically one in 42 boys. Despite the 15% increase in prevalence in the last two years, there is no specific etiology, objective diagnostic criteria, or drug treatment. However, up-regulation of inflammation in ASD patients has been demonstrated in blood samples. Increased peripheral inflammation could have devastating effects on the developing brain. Peripheral inflammation in the blood could cross the blood-brain-barrier to stimulate microglia in the brain to produce aberrant levels of cytokines that regulate neuroinflammation such as insulin-like growth factor one (IGF1) that could alter neuronal cell-surface expression and neurotransmission. Additionally, arginase serves as a marker of inflammation, produced and expressed during cellular remodeling during brain injury. A balance of neurotransmitters, glutamate and gamma-aminobutyric acid (GABA), is critical to facilitate inter-regional signaling in the brain. Alterations of inflammatory molecules and the effects on glutamatergic neurons ability to uptake GABA in certain brain areas is currently unknown in ASD. Pathological changes in brain areas associated with social behaviors have been identified in postmortem tissue from ASD donors when compared to typically developing (TD) age and gender matched control tissue, as well as, in imaging scans of living individuals with ASD. We hypothesize that expression of inflammatory related molecules are increased in the identified brain areas related to symptoms of ASD and can be associated with altered gene expression changes in neurons as shown by gamma-aminobutyric acid type A receptor alpha 1 subunit (GABRA1). Dysfunction of GABRA1 on glutamatergic neurons could disrupt the typical neuronal balance of glutamate and GABA signaling. Inflammatory markers, IGF1 and insulin-like growth factor one receptor (IGF1R), were evaluated using quantitative polymerase chain reaction (QPCR). Additionally, IGF1 and arginase were evaluated using immunohistochemistry in both white and gray matter from the anterior cingulate cortex (ACC). Laser capture microdissection (LCM) was used to obtain single cell captures of glutamatergic neurons. IGF1R and GABRA1 gene expression was measured using end point PCR. A significant increase in IGF1 expression was obtained in the white matter punch in comparison to typically developed age-matched subjects using QPCR during initial statistical significance, however, was ultimately not significant. Additionally, IGF1R expression was significantly increased in ASD neurons in comparison to TD subjects utilizing the LCM method. However, a decrease expression in GABRA1 trended significance indicating a possible alteration in the neuron’s ability to facilitate proper signaling. These findings are the foundation of future investigations of signaling pathways in ASD that may uncover cell-specific etiologies and drug therapies for a condition that is only projected to increase in prevalence.

The number of children diagnosed with autism spectrum disorder (autism) has steadily increased dramatically over the past generation, and more students with autism than ever before are enrolled in the public education system. Educating students with autism presents unique challenges (e.g., shortage of staff, low incidence of autism, limited programming) to rural school districts. Rural districts must adhere to the same federal and state guidelines (e.g., Individuals with Disabilities Education Act & Free and Appropriate Public Education) as urban districts that have more readily available resources in providing appropriate programming. This study examined stakeholders' perceptions of the current services offered in the targeted rural district including effectiveness of such resources. Fifty one stakeholders participated, including general education/special education teachers, related services providers, administration, parents, and students diagnosed with autism. Research questions were accessed through an online survey with the option of a follow up interview that addressed perceptions of current accommodations and modifications implemented in the general education classroom and their overall effectiveness. The data was analyzed by mixed methods, including both qualitative and quantitative data. The findings from stakeholders presented four common themes: (a) increased trainings for stakeholders; (b) a need to improve collaboration amongst all school staff including communication with parents of autistic students; (c) enhanced Child Find through early identification of autistic students; and (d) access to additional resources within the rural school and the community. Immediate recommendations for the rural district include: (a) web-based training options through email, school newsletters, inservice, and on the district's special education site; (b) forming a quarterly focus and/or support group with parents, educators, and administration to strengthen the partnership between the school and the community; (c) initiating conversations with local pediatric offices to implement early identification autism screening tools; and (d) collaboration with the Utah Parent Center to organize parent meetings/trainings. Additionally, the Local Education Agency (LEA) should continue to utilize regional itinerant supports and explore options to increase these services for the district. An executive summary was presented to the local school board to guide future decisions regarding the needs of students with autism as well as improve the outcomes and quality of their lives.

Autism spectrum disorder (ASD) is considered a disease of neuronal dysfunction based on pathological alterations in axon thickness and neuronal disorganization. Recent findings suggest non-neuronal cells may also play a role in ASD brain pathology. White matter areas in the ASD brain display enlargement paired with a reduction in structural integrity. These structural abnormalities are likely associated with dysfunction of the most prevalent cell types present in white matter, astrocytes and oligodendrocytes. In fact, myelin abnormalities and structural changes of reactive astrocytes have been reported in ASD. The goal of the present study was to further investigate glia pathology in the white matter of the ASD brain. The primary brain area of interest was the anterior cingulate cortex (BA24) because this brain region mediates social interactive behavior, disruption of which is a core behavioral feature of ASD. Furthermore, a reduction in the structural integrity of white matter in BA24 has been observed in ASD. Postmortem brain tissues were obtained from highly characterized ASD and developmentally normal control donors. Quantitative Western blotting was used to measure glial fibrillary acidic protein (GFAP) and myelin oligodendrocyte glycoprotein (MOG) produced by astrocytes and oligodendrocytes, respectively. A significant elevation in levels of GFAP-immunoreactivity (p=0.005) in BA24 white matter was observed in ASD as compared to control donors. In contrast, levels of MOG-immunoreactivity in BA24 white matter were similar when comparing ASD to control donors. Levels of both GFAP and MOG in the BA24 gray matter from the same subjects were similar comparing the two groups of donors. Measurement of GFAP gene expression in BA24 white matter did not reveal any difference between ASD and control donors. To further examine the regional specificity of the observed glial pathology, we analyzed GFAP and MOG protein expression in the anterior prefrontal cortex (BA10) white matter. Levels of GFAP- and MOG-immunoreactivities were unchanged in BA10 white matter comparing ASD to control donors. These findings demonstrate that astrocytic pathology is both tissue-specific (white matter) and regionally selective (BA24) in ASD. Elevation of GFAP protein in BA24 white matter implies an activation of astrocytes possibly as a result of a yet undefined cellular insult. Research is needed to investigate the molecular pathways that underlie this astrocyte reaction and such research may yield important clues regarding the etiology of ASD.

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Research into the cause of autism continues without any clear-cut answers. However, recent studies suggest that abnormalities of the immune system are associated with this disorder and autism results from failure of the immune system to regulate itself. Proper immune regulation requires that the host have the appropriate number and percentage of each population of lymphocytes and monocytes. These populations can be distinguished from one another with monoclonal antibodies that react with unique protein structures on the cell surface designated as the "cluster of differentiation" (CD) antigens. This investigation studied the possibility that the immune abnormalities seen in autism are due to a change in the lymphocytes or monocytes in the subjects with autism . The autistic subjects as compared to age- and sex-matched control subjects exhibited several changes in their cell populations. These included a depression of total lymphocytes, CD2+ (total T cells), CD4+ (helper T cells), and CD4+CD45RA+ (the antigen-inexperienced, suppressor inducer subset of helper T cells). Also analyzed were the siblings of the autistic subjects. A reduced percentage of CD4+ cells was seen in the male siblings as compared to unrelated males. Analyses also compared the cells of mothers and fathers of the autistic subjects with controls of mothers and fathers of normal children. No differences were seen in any of the markers used. Findings in the literature show an increase in memory cells and a decrease in naive cells as a function of age. The data gathered in these experiments uphold this concept and are consistent with the idea that CD45RA and CDw29 are maturational states of helper T cells. The quantitation of different immune markers on lymphoid cells seems to have been useful in the further characterization and investigation of the immune mechanism relevant to the syndrome of autism. Differences in some of the cell types were observed and may account for some of the immune abnormalities seen in autism. These differences may be the result or the cause of the syndrome. Further investigation seems necessary before a direct pathological link can be found between the body's immunity and autism.

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Bright Mosaic is a 30-minute documentary about a comprehensive autism center for children with an organic and unconventional approach. The Bright Mosaic Autism Therapy Center's exceptional curriculum consists of a mix of Montessori practices, natural sciences, applied behavior analysis, occupational therapy, speech therapy, physical therapy, play therapy, music therapy, sensory integration, daily life skills and art. Bright Mosaic mixes observational and participatory styles in an effort to portray an exceptionally skilled and passionate team who fights a tough daily battle to prepare their children for the life ahead of them.

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