1. Anderson-Hanley C, Tureck K, Schneiderman RL. {{Autism and exergaming: effects on repetitive behaviors and cognition}}. {Psychol Res Behav Manag};2011;4:129-137.
Autism is a neurodevelopmental disorder that leads to impairment in social skills and delay in language development, and results in repetitive behaviors and restricted interests that impede academic and social involvement. Physical exercise has been shown to decrease repetitive behaviors in autistic children and improve cognitive function across the life-span. Exergaming combines physical and mental exercise simultaneously by linking physical activity movements to video game control and may yield better compliance with exercise. In this investigation, two pilot studies explored the potential behavioral and cognitive benefits of exergaming. In Pilot I, twelve children with autism spectrum disorders completed a control task and an acute bout of Dance Dance Revolution (DDR); in Pilot II, ten additional youths completed an acute bout of cyber cycling. Repetitive behaviors and executive function were measured before and after each activity. Repetitive behaviors significantly decreased, while performance on Digits Backwards improved following the exergaming conditions compared with the control condition. Additional research is needed to replicate these findings, and to explore the application of exergaming for the management of behavioral disturbance and to increase cognitive control in children on the autism spectrum.
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2. Auerbach BD, Osterweil EK, Bear MF. {{Mutations causing syndromic autism define an axis of synaptic pathophysiology}}. {Nature};2011 (Nov 23)
Tuberous sclerosis complex and fragile X syndrome are genetic diseases characterized by intellectual disability and autism. Because both syndromes are caused by mutations in genes that regulate protein synthesis in neurons, it has been hypothesized that excessive protein synthesis is one core pathophysiological mechanism of intellectual disability and autism. Using electrophysiological and biochemical assays of neuronal protein synthesis in the hippocampus of Tsc2(+/-) and Fmr1(-/y) mice, here we show that synaptic dysfunction caused by these mutations actually falls at opposite ends of a physiological spectrum. Synaptic, biochemical and cognitive defects in these mutants are corrected by treatments that modulate metabotropic glutamate receptor 5 in opposite directions, and deficits in the mutants disappear when the mice are bred to carry both mutations. Thus, normal synaptic plasticity and cognition occur within an optimal range of metabotropic glutamate-receptor-mediated protein synthesis, and deviations in either direction can lead to shared behavioural impairments.
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3. Critchfield JW, van Hemert S, Ash M, Mulder L, Ashwood P. {{The potential role of probiotics in the management of childhood autism spectrum disorders}}. {Gastroenterol Res Pract};2011;2011:161358.
Gastrointestinal (GI) dysfunction has been reported in a substantial number of children with autism spectrum disorders (ASD). Activation of the mucosal immune response and the presence of abnormal gut microbiota are repeatedly observed in these children. In children with ASD, the presence of GI dysfunction is often associated with increased irritability, tantrums, aggressive behaviour, and sleep disturbances. Moreover, modulating gut bacteria with short-term antibiotic treatment can lead to temporary improvement in behavioral symptoms in some individuals with ASD. Probiotics can influence microbiota composition and intestinal barrier function and alter mucosal immune responses. The administration of probiotic bacteria to address changes in the microbiota might, therefore, be a useful novel therapeutic tool with which to restore normal gut microbiota, reduce inflammation, restore epithelial barrier function, and potentially ameliorate behavioural symptoms associated with some children with ASD. In this review of the literature, support emerges for the clinical testing of probiotics in ASD, especially in the context of addressing GI symptoms.
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4. De Felice C, Maffei S, Signorini C, Leoncini S, Lunghetti S, Valacchi G, D’Esposito M, Filosa S, Della Ragione F, Butera G, Favilli R, Ciccoli L, Hayek J. {{Subclinical myocardial dysfunction in Rett syndrome}}. {Eur J Echocardiogr};2011 (Nov 23)
AIMS: Rett syndrome (RTT) is a rare neurodevelopmental disorder frequently linked to methyl-CpG-binding protein 2 (MeCP2) gene mutations. RTT is associated with a 300-fold increased risk of sudden cardiac death. Rhythm abnormalities and cardiac dysautonomia do not to fully account for cardiac mortality. Conversely, heart function in RTT has not been explored to date. Recent data indicate a previously unrecognized role of MeCP2 in cardiomyocytes development. Besides, increased oxidative stress markers (OS) have been found in RTT. We hypothesized that (i) RTT patients present a subclinical biventricular dysfunction and (ii) the myocardial dysfunction correlate with OS. METHODS AND RESULTS: We evaluated typical (n = 72) and atypical (n = 20) RTT female and healthy controls (n = 92). Main outcome measurements were (i) echocardiographic biventricular systo-diastolic parameters; (ii) correlation between echocardiographic measures and OS levels, i.e. plasma and intra-erythrocyte non-protein-bound iron (NPBI) and plasma F2-Isoprostanes (F2-IsoPs).A significant reduction in longitudinal biventricular function (tricuspid annular plane systolic excursion, mitral annular plane systolic excursion, S’ of lateral and septal mitral annulus, S’ of tricuspidal annulus) was evidenced in RTT patients vs. controls. No significant changes in the LV ejection fraction were found. Peak-early filling parameters (E, E’ of lateral mitral annulus, E’ of tricuspidal annulus) and right ventricular systolic pressure were reduced. A-wave, E/A, and E/E’ were normal. OS markers were increased, but only F2-IsoPs correlated to LV systolic dysfunction. CONCLUSION: These data indicate a previously unrecognized subclinical systo-diastolic biventricular myocardial dysfunction in typical and atypical RTT patients. A reduced preload is evidenced. The biventricular dysfunction is partially related to OS damage.
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5. Graf M. {{Smart approach to testing needed for fragile X syndrome}}. {Manag Care};2011 (Oct);20(10):70-72.
6. Hudson M, Burnett HG, Jellema T. {{Anticipation of Action Intentions in Autism Spectrum Disorder}}. {J Autism Dev Disord};2011 (Nov 24)
We investigated whether individuals with a mild form of autism spectrum disorder (ASD) are influenced by an actor’s gaze direction when anticipating how an observed action will continue in the immediate future. Participants observed a head rotate towards them, while the gaze direction was either leading, or lagging behind, rotation. They also observed identical rotations of a cylinder containing the geometrical equivalent of the gaze manipulation. The control group was influenced by the gaze manipulations for the animate but not the inanimate stimulus. The ASD group did not discriminate between the stimuli, showing a similar influence for both. This suggests that the ASD responses in the animate condition were biased by the low-level directional features of the eyes rather than by the conveyed intentions.
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7. Russell G, Golding J, Norwich B, Emond A, Ford T, Steer C. {{Social and behavioural outcomes in children diagnosed with autism spectrum disorders: a longitudinal cohort study}}. {J Child Psychol Psychiatry};2011 (Nov 23)
Objective: To compare social and behavioural outcomes between children formally diagnosed with autism spectrum disorders (ASD) with those of children who displayed autistic traits at preschool age, but remained undiagnosed as teenagers. Method: A secondary analysis of data from a birth cohort study, the Avon Longitudinal Study of Parents and Children (N = 13,944), in SW England. Children clinically diagnosed with ASD were identified from their medical records (n = 71). A comparison group, who displayed autistic traits at age 3-4, but without ASD diagnosis were also identified (n = 142). Social and behavioural outcomes in adolescence were compared between the two groups. Results: Children with ASD diagnoses were more impaired as teenagers that those in the comparison group on a range of measures of autistic-like behaviour. The developmental trajectory of prosocial behaviour showed that differences between the case and comparison groups increased dramatically in the preschool and early primary years, but that after 6 years the trajectories were similar. Conclusions: The divergence of the clinically diagnosed group and the nondiagnosed group in measures of autistic-like behaviour increased with age. This study provides evidence that it may be difficult to distinguish preschool age children who exhibit autistic-like symptoms but improve, from those who go on to develop lifelong impairment.
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8. Tamada K, Nakai N, Takumi T. {{[A humanized mouse model of autism]}}. {Seikagaku};2011 (Sep);83(9):841-845.
