1. Ghanizadeh A. {{Malondialdehyde, Bcl-2, Superoxide Dismutase and Glutathione Peroxidase may Mediate the Association of Sonic Hedgehog Protein and Oxidative Stress in Autism}}. {Neurochem Res};2011 (Dec 6)
Sonic hedgehog signaling and brain-derived neurotrophic factor play a neuro-protective role against oxidative stress in autism. Sonic hedgehog also increases Bcl-2 expression and the activities of superoxide dismutase and glutathione peroxidase. The level or activity of Bcl-2, brain-derived neurotrophic factor, and the activities of superoxide dismutase and glutathione peroxidase are decreased in autism. Sonic hedgehog also decreases the production of malondialdehyde that its level is high in autism. Therefore, it is supposed that sonic hedgehog may be associated with oxidative stress in autism through other pathways too.
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2. Ingersoll B. {{Brief Report: Effect of a Focused Imitation Intervention on Social Functioning in Children with Autism}}. {J Autism Dev Disord};2011 (Dec 7)
Imitation is an early skill thought to play a role in social development, leading some to suggest that teaching imitation to children with autism should lead to improvements in social functioning. This study used a randomized controlled trial to evaluate the effect of a focused imitation intervention on initiation of joint attention and social-emotional functioning in 27 young children with autism. Results indicated the treatment group made significantly more gains in joint attention initiations at post-treatment and follow-up and social-emotional functioning at follow-up than the control group. Although gains in social functioning were associated with treatment, a mediation analysis did not support imitation as the mechanism of action. These findings suggest the intervention improves social functioning in children with ASD.
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3. Rossignol DA, Frye RE. {{A review of research trends in physiological abnormalities in autism spectrum disorders: immune dysregulation, inflammation, oxidative stress, mitochondrial dysfunction and environmental toxicant exposures}}. {Mol Psychiatry};2011 (Dec 6)
Recent studies have implicated physiological and metabolic abnormalities in autism spectrum disorders (ASD) and other psychiatric disorders, particularly immune dysregulation or inflammation, oxidative stress, mitochondrial dysfunction and environmental toxicant exposures (‘four major areas’). The aim of this study was to determine trends in the literature on these topics with respect to ASD. A comprehensive literature search from 1971 to 2010 was performed in these four major areas in ASD with three objectives. First, publications were divided by several criteria, including whether or not they implicated an association between the physiological abnormality and ASD. A large percentage of publications implicated an association between ASD and immune dysregulation/inflammation (416 out of 437 publications, 95%), oxidative stress (all 115), mitochondrial dysfunction (145 of 153, 95%) and toxicant exposures (170 of 190, 89%). Second, the strength of evidence for publications in each area was computed using a validated scale. The strongest evidence was for immune dysregulation/inflammation and oxidative stress, followed by toxicant exposures and mitochondrial dysfunction. In all areas, at least 45% of the publications were rated as providing strong evidence for an association between the physiological abnormalities and ASD. Third, the time trends in the four major areas were compared with trends in neuroimaging, neuropathology, theory of mind and genetics (‘four comparison areas’). The number of publications per 5-year block in all eight areas was calculated in order to identify significant changes in trends. Prior to 1986, only 12 publications were identified in the four major areas and 51 in the four comparison areas (42 for genetics). For each 5-year period, the total number of publications in the eight combined areas increased progressively. Most publications (552 of 895, 62%) in the four major areas were published in the last 5 years (2006-2010). Evaluation of trends between the four major areas and the four comparison areas demonstrated that the largest relative growth was in immune dysregulation/inflammation, oxidative stress, toxicant exposures, genetics and neuroimaging. Research on mitochondrial dysfunction started growing in the last 5 years. Theory of mind and neuropathology research has declined in recent years. Although most publications implicated an association between the four major areas and ASD, publication bias may have led to an overestimation of this association. Further research into these physiological areas may provide insight into general or subset-specific processes that could contribute to the development of ASD and other psychiatric disorders.Molecular Psychiatry advance online publication, 6 December 2011; doi:10.1038/mp.2011.165.
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4. Roth DA, Muchnik C, Shabtai E, Hildesheimer M, Henkin Y. {{Evidence for atypical auditory brainstem responses in young children with suspected autism spectrum disorders}}. {Dev Med Child Neurol};2011 (Dec 5)
Aim The aim of this study was to characterize the auditory brainstem responses (ABRs) of young children with suspected autism spectrum disorders (ASDs) and compare them with the ABRs of children with language delay and with clinical norms. Method The ABRs of 26 children with suspected ASDs (21 males, five females; mean age 32.5mo) and an age- and sex-matched group of 26 children with language delay (22 males, four females) were analysed. All children had normal hearing. The absolute latencies of waves I, III, and V, and interpeak latencies (IPLs) I to III, I to V, and III to V of the group with ASDs and the group with language delay were compared. Data from both groups were further compared with clinical norms. Results All absolute latencies and IPLs were significantly prolonged in the group with suspected ASDs compared with the group with language delay, excluding IPL III-V (all p-values <0.05) and with clinical norms (all p-values <0.001; IPL III-V, p<0.05). Significant prolongation of absolute and IPLs was also evident in the group with language delay compared with clinical norms, excluding IPL III to V (all p-values <0.001). The prevalence of abnormal findings in two or more absolute latencies was found to be significantly higher in the group with ASDs (50%) than in the group with language delay (8%; p=0.002). Interpretation The results provide first-time evidence for a neurodevelopmental brainstem abnormality that is already apparent in young children with suspected ASD and language delay. The overlap in ABR findings supports the assertion that an auditory processing deficit may be at the core of these two disorders.
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5. Saugstad LF. {{Infantile autism: a chronic psychosis since infancy due to synaptic pruning of the supplementary motor area}}. {Nutr Health};2011;20(3-4):171-182.
The rise in infantile autism, learning problems, cognitive decline with age, Alzheimer’s, Parkinson’s diseases and the SIDS epidemic, has a common cause in the rising dietary deficit in Omega-3 brain-food. This paper suggests that aside from the wider concept of autism spectrum disorders (ASD) and pervasive developmental disorders (PDD), the rise in infantile autism (IA) in the last decade is the effect of deficient brain-food (Omega-3). The consequent delay of development, prolongs the 2nd regressive event in infancy to pruning of the centre in the Medial Frontal Lobe System that connects hippocampus and singulum. With a consequently defective supplementary motor area (SMA), the Delayed Response Function is affected leading to persistent psychosis. Post-pubertal episodic psychoses are associated with acute reduction of excitation, a risk of breakdown of circuitry, insufficient fill-in mechanisms, and silent spots. An acute psychosis occurs if the silent spots compromise SMA. Only two brain areas have continuous neurogenesis, indicating their important functions: the Hippocampus and Olfactory Bulb that belongs to the lateral frontal lobe system essential to survival. Concerned with necessity of action in response to the environment, it relies upon short-term memory and acute feedback mechanisms influenced by emotion and motivation from the external world. In contrast, the medial frontal lobe network is controlled by feed-forward predictive mechanisms related to storage of information The Delayed Response Function is mastered at 7 months, when 2nd event occurs with pruning of axons and dendrites. An abolished or defective delayed response function seriously incapacitates an individual: a defective « social brain » with an inability for conscious action and to communicate, predominates in IA. There is a near lack of speech, despite normal vision and hearing in the minority without marked adversity in pregnancy, at delivery or in infancy. The recent rise in IA despite no rise in adversity signifies a rising deficiency in brain-food. This is suggested by a changing clinical picture: no Mental Retardation in an IA majority. Deficit in olfaction is pathognomonic in schizophrenia since 30 yrs and distinguishes the Asperger syndrome. If brain-food deficiency alone sufficiently prolongs pruning to cause absent activity in SMA in infancy, less mentally retarded IA from other causes might be observed. Deficit in brain-food was evident in the Sudden Infant Death Syndrome: birthweight averaged 200-300g lower than sibs, Omega-3 levels in brainstem were lower than controls. Only 20% SIDS died in first hypoxic episode, suggesting such episodes are more frequent than we imagined. Children with learning-behaviour problems have similarly depressed birthweight. A general deficiency in omega-3 contributes to the lacking reduction in Schizophrenia, despite early puberty predominates. Olfactory bulb is first affected in the Alzheimer’s and Parkinson’s disease. Cognitive decline with age, hippocampal dysfunctions rises markedly irrespective of disease, but the major mental illnesses and Infantile Autism in particular, benefit from « brainfood » that might also prevent a development of these disorders. To secure optimal brain function in the coming generations, there is a need to change the diet now from its emphasis on protein for body growth to food for the brain. This means there is a need to increase fish and sea food consumption.
6. Schanding GT, Jr., Nowell KP, Goin-Kochel RP. {{Utility of the Social Communication Questionnaire-Current and Social Responsiveness Scale as Teacher-Report Screening Tools for Autism Spectrum Disorders}}. {J Autism Dev Disord};2011 (Dec 6)
Limited research exists regarding the role of teachers in screening for Autism Spectrum Disorders (ASD). The current study examined the use of the Social Communication Questionnaire (SCQ) and Social Responsiveness Scale (SRS) as completed by parents and teachers about school-age children from the Simons Simplex Collection. Using the recommended cutoff scores in the manuals and extant literature, the teacher-completed SCQ and SRS yielded lower sensitivity and specificity values than would be desirable; however, lowering the cutoff scores on both instruments improved sensitivity and specificity to more adequate levels for screening purposes. Using the adjusted cutoff scores, the SRS teacher form appears to be a slightly better screener than the SCQ. Implications and limitations are discussed, as well as areas for future research.
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7. Ververi A, Vargiami E, Papadopoulou V, Tryfonas D, Zafeiriou DI. {{Clinical and Laboratory Data in a Sample of Greek Children with Autism Spectrum Disorders}}. {J Autism Dev Disord};2011 (Dec 7)
The purpose of this study is to describe clinical and laboratory data, as well as comorbid disorders in Greek children with autism spectrum disorders (ASD). Data were retrospectively collected for 222 children aged 1.5-9 years. The mean age at diagnosis was 43.7 +/- 17.6 months. Significantly earlier diagnoses were noted in children with comorbid disorders (epilepsy, hearing deficits, genetic/metabolic disorders), mental retardation and a large head circumference (HC). Macrocephaly (HC >/= 97th percentile) was found in 21.2% of children, genetic and metabolic disorders in 11.7% and 2.7% respectively and mental retardation in 23%. Patients with certain clinical features (i.e. syndromic) are earlier diagnosed. It is of ultimate importance to promptly identify all children with ASD, probably through the appliance of screening and surveillance programs in the Greek population.
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8. Wild KS, Poliakoff E, Jerrison A, Gowen E. {{Goal-Directed and Goal-Less Imitation in Autism Spectrum Disorder}}. {J Autism Dev Disord};2011 (Dec 7)
To investigate how people with Autism are affected by the presence of goals during imitation, we conducted a study to measure movement kinematics and eye movements during the imitation of goal-directed and goal-less hand movements. Our results showed that a control group imitated changes in movement kinematics and increased the level that they tracked the hand with their eyes, in the goal-less compared to goal-direction condition. In contrast, the ASD group exhibited more goal-directed eye movements, and failed to modulate the observed movement kinematics successfully in either condition. These results increase the evidence for impaired goal-less imitation in ASD, and suggest that there is a reliance on goal-directed strategies for imitation in ASD, even in the absence of visual goals.
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9. Zmigrod S, de Sonneville LM, Colzato LS, Swaab H, Hommel B. {{Cognitive control of feature bindings: evidence from children with autistic spectrum disorder}}. {Psychol Res};2011 (Dec 6)
Understanding how the brain integrates features from different domains that are processed in distinct cortical regions calls for the examination of integration processes. Recent studies of feature-repetition effects demonstrated interactions across perceptual features and action-related features: repeating only some features of the perception-action episode hinders performance. These partial-repetition costs point to the existence of temporary memory traces (event files). However, the principles and the constraints that govern the management of such traces are still unclear. Here, we investigated whether children with autistic spectrum disorder (ASD) differ from typically developing children in managing episodic memory traces. The results show that both groups integrate stimulus features along with action features, but children with ASD exhibit larger partial-repetition costs, suggesting lesser control and flexibility in updating episodic memory traces. The findings are discussed in the light of evidence for a central role of the dopaminergic system in cognitive integration, ASD, and cognitive control.
