1. Ahn Y, Narous M, Tobias R, Rho JM, Mychasiuk R. {{The Ketogenic Diet Modifies Social and Metabolic Alterations Identified in the Prenatal Valproic Acid Model of Autism Spectrum Disorder}}. {Developmental neuroscience}. 2014 Jul 8.
Autism spectrum disorder (ASD) is a highly prevalent neurodevelopmental disorder characterized by abnormal social interactions, communication deficits and stereotyped or repetitive behaviors. Although the etiology of ASD remains elusive, converging lines of research indicate that mitochondrial dysfunction may play a substantive role in disease pathophysiology. Without an established causal link, the generation of therapeutic targets for ASD has been relatively unsuccessful and has focused solely on individual symptoms. The ketogenic diet (KD) is a high-fat low-carbohydrate diet that has previously been used for the treatment of intractable epilepsy and is known to enhance mitochondrial function. The purpose of this study was to determine if the KD could reverse the social deficits and mitochondrial dysfunction identified in the prenatal valproic acid (VPA) rodent model of ASD. Sprague-Dawley dams were administered VPA or saline on gestational day 12.5. The pups were treated with the KD or their standard diet (SD) for 10 days beginning on postnatal day 21 (PD21). On PD35 juvenile play behavior was tested with the play-fighting paradigm and rats were then sacrificed for mitochondrial bioenergetic analysis. The offspring exposed to VPA prenatally demonstrated a significant decrease in the number of play initiations/attacks and this was reversed with the KD. Prenatal VPA exposure also disrupted the pattern of play responses; VPA/SD animals used complete rotations more often than saline control animals. Treatment with the KD did not affect the number of complete rotations. In addition, while prenatal exposure to VPA altered mitochondrial respiration, the KD was able to restore aspects of bioenergetic dysfunction. As the KD was able to modify complex social behaviors and mitochondrial respiration, it may be a useful treatment option for ASD. Future studies will need to examine the effectiveness of the KD to reverse the two additional core deficits of ASD and to explore various treatment regimens to determine optimal treatment duration and formulation. (c) 2014 S. Karger AG, Basel.
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2. Berger NI, Ingersoll B. {{A Further Investigation of Goal-Directed Intention Understanding in Young Children with Autism Spectrum Disorders}}. {Journal of autism and developmental disorders}. 2014 Jul 8.
Findings from research investigating goal-directed intention understanding in children with autism spectrum disorders (ASD) have been equivocal, in part because of the varying methodologies used across studies. This study compares both object-oriented and social-communicatively cued goal-directed intention understanding in children with ASD and typically-developing children. Relative to matched controls, children with ASD did not exhibit deficits in object-oriented intention understanding. While children with ASD also demonstrated the ability to understand intention when cued by social-communication indicators, typically-developing children differentiated between intentional and unintentional acts at a significantly greater level. Group differences in performance were eliminated if only trials in which children attended to the experimenter’s face were considered. Results suggest that children with ASD have intact object-oriented intention understanding abilities, and are able to use social-communicative cues to understand intention. However, their ability to demonstrate social-communicatively cued intention understanding is limited by a lack of attention to relevant social-communicative information.
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3. Bernier R, Golzio C, Xiong B, Stessman HA, Coe BP, Penn O, Witherspoon K, Gerdts J, Baker C, Vulto-van Silfhout AT, Schuurs-Hoeijmakers JH, Fichera M, Bosco P, Buono S, Alberti A, Failla P, Peeters H, Steyaert J, Vissers LE, Francescatto L, Mefford HC, Rosenfeld JA, Bakken T, O’Roak BJ, Pawlus M, Moon R, Shendure J, Amaral DG, Lein E, Rankin J, Romano C, de Vries BB, Katsanis N, Eichler EE. {{Disruptive CHD8 Mutations Define a Subtype of Autism Early in Development}}. {Cell}. 2014 Jul 3.
Autism spectrum disorder (ASD) is a heterogeneous disease in which efforts to define subtypes behaviorally have met with limited success. Hypothesizing that genetically based subtype identification may prove more productive, we resequenced the ASD-associated gene CHD8 in 3,730 children with developmental delay or ASD. We identified a total of 15 independent mutations; no truncating events were identified in 8,792 controls, including 2,289 unaffected siblings. In addition to a high likelihood of an ASD diagnosis among patients bearing CHD8 mutations, characteristics enriched in this group included macrocephaly, distinct faces, and gastrointestinal complaints. chd8 disruption in zebrafish recapitulates features of the human phenotype, including increased head size as a result of expansion of the forebrain/midbrain and impairment of gastrointestinal motility due to a reduction in postmitotic enteric neurons. Our findings indicate that CHD8 disruptions define a distinct ASD subtype and reveal unexpected comorbidities between brain development and enteric innervation.
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4. Canitano R. {{New experimental treatments for core social domain in autism spectrum disorders}}. {Frontiers in pediatrics}. 2014;2:61.
Current therapeutics in autism spectrum disorders (ASD) only treat the associated symptoms, without addressing core social dysfunctions. A paradigm shift in research of the pathogenesis of ASD, its synaptic abnormalities and altered signaling in multiple dynamic systems, have led to new experimental treatments for treating the core social abnormalities of ASD. NMDA antagonists, especially memantine, have been introduced in clinical trials addressing glutamatergic transmission in children and adolescents with ASD. GABAergic signaling has been targeted in trials using the GABAB receptor agonist arbaclofen for ASD patients with promising results. Oxytocin has been recognized as implicated in social development and affiliative behaviors. Preliminary findings from clinical trials using oxytocin in children with ASD show encouraging improvements in social cognition, but larger studies are needed. In two of the single gene disorders associated with ASD, Insulin Growth Factor (IGF-1) is a new treatment that has been tested in Rett syndrome and Phelan-McDermid syndrome (Chromosome 22 deletion syndrome). IGF-1 has been demonstrated to reverse the reduction in the number of excitatory synapses and the density of neurons that characterize these conditions in animal studies and it is being introduced as an experimental treatment. As a novel approach to verify treatment efficacy, neural processing modifications were recently evaluated by fMRI after a pivotal response training intervention. Another study of neural changes in response to treatment examined variations in EEG signaling in patients after an Early Start Denver Model (ESDM) intervention.
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5. Carnerero JJ, Perez-Gonzalez LA. {{Induction of naming after observing visual stimuli and their names in children with autism}}. {Research in developmental disabilities}. 2014 Jul 8;35(10):2514-26.
A novel procedure to induce pairing naming, considered the emergence of tacts and selection of pictures after observing names and its corresponding pictures without specific consequences, was probed in 4 persons with autism who lacked this capability with a multiple probe design across participants. Five pictures were selected per set. The participants observed the pictures on a computer screen while the experimenter said the name of the picture. Then, the emission of untaught uninstructed tacts of the pictures was tested without reinforcement. The cycle was repeated until a criterion of 90% correct responses was achieved. Thereafter, in probes without reinforcement, the participants tacted the pictures without specific instructions and also when asked to name them, and selected the correct picture upon hearing their names. The procedure was repeated with two additional stimulus sets and the probed relations emerged always. Two children showed the emergence with fewer trials across sets, which indicate emergence induction. Thus, the procedure served to test whether the pairing naming capability was missing and induced the capability. The results may have important utility in teaching persons diagnosed with autism and other learning difficulties and for accelerating learning in all children.
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6. Castro J, Garcia RI, Kwok S, Banerjee A, Petravicz J, Woodson J, Mellios N, Tropea D, Sur M. {{Functional recovery with recombinant human IGF1 treatment in a mouse model of Rett Syndrome}}. {Proceedings of the National Academy of Sciences of the United States of America}. 2014 Jul 8;111(27):9941-6.
Rett Syndrome is a neurodevelopmental disorder that arises from mutations in the X-linked gene methyl-CpG binding protein 2 (MeCP2). MeCP2 has a large number of targets and a wide range of functions, suggesting the hypothesis that functional signaling mechanisms upstream of synaptic and circuit maturation may contribute to our understanding of the disorder and provide insight into potential treatment. Here, we show that insulin-like growth factor-1 (IGF1) levels are reduced in young male Mecp2-null (Mecp2(-/y)) mice, and systemic treatment with recombinant human IGF1 (rhIGF1) improves lifespan, locomotor activity, heart rate, respiration patterns, and social and anxiety behavior. Furthermore, Mecp2-null mice treated with rhIGF1 show increased synaptic and activated signaling pathway proteins, enhanced cortical excitatory synaptic transmission, and restored dendritic spine densities. IGF1 levels are also reduced in older, fully symptomatic heterozygous (Mecp2(-/+)) female mice, and short-term treatment with rhIGF1 in these animals improves respiratory patterns, reduces anxiety levels, and increases exploratory behavior. In addition, rhIGF1 treatment normalizes abnormally prolonged plasticity in visual cortex circuits of adult Mecp2(-/+) female mice. Our results provide characterization of the phenotypic development of Rett Syndrome in a mouse model at the molecular, circuit, and organismal levels and demonstrate a mechanism-based therapeutic role for rhIGF1 in treating Rett Syndrome.
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7. Chen CH, Huang CC, Cheng MC, Chiu YN, Tsai WC, Wu YY, Liu SK, Gau SS. {{Genetic analysis of GABRB3 as a candidate gene of autism spectrum disorders}}. {Molecular autism}. 2014;5:36.
BACKGROUND: GABRB3 is a position candidate gene at chromosome 15q12 that has been implicated in the neurobiology of autism spectrum disorders (ASD). The aim of this study was to examine the genetic association of GABRB3 with ASD. METHODS: The sample consisted of 356 patients with clinical diagnosis of ASD according to the DSM-IV diagnostic criteria and confirmed by the Autism Diagnostic Interview-Revised and 386 unrelated controls. We searched for mutations at all the exonic regions and 1.6 Kb of the 5′ region of GABRB3 in the genomic DNA of all the participants using the Sanger sequencing. We implemented a case-control association analysis of variants detected in this sample, and conducted a reporter gene assay to assess the functional impact of variants at the 5′ regulatory region. RESULTS: We detected six known common SNPs; however, they were not associated with ASD. Besides, a total of 22 rare variants (12 at 5′ regulatory, 4 at intronic, and 6 at exonic regions) were detected in 18 patients and 6 controls. The frequency of rare variants was significantly higher in the patient group than in the control group (18/356 versus 6/386, odds ratio = 3.37, P = 0.007). All the 12 rare variants at the 5′ regulatory region were only detected in 7 patients, but not in any of the controls (7/356 versus 0/386, Fisher’s exact test, P = 0.006). Two patients carried multiple rare variants. Family studies showed that most of these rare variants were transmitted from their parents. Reporter gene assays revealed that four rare variants at the 5′ regulatory region and 1 at exon 1a untranslated region had elevated reporter gene activities compared to two wild type alleles. CONCLUSIONS: Our data suggest rare variants of GABRB3 might be associated with ASD, and increased GABRB3 expression may contribute to the pathogenesis of ASD in some patients. TRIAL REGISTRATION: CLINICAL TRIAL REGISTRATION IDENTIFIER: NCT00494754.
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8. Daley TC, Weisner T, Singhal N. {{Adults with autism in India: A mixed-method approach to make meaning of daily routines}}. {Social science & medicine (1982)}. 2014 Jul 1;116C:142-9.
Although individuals with Autism Spectrum Disorder (ASD) have been diagnosed in India for over fifty years, virtually nothing is known about the social circumstances of adults, their daily lives, and their families. Where are adults with autism? How do they spend their time? Who are they with, and what are they doing all day? A mixed-method approach was used to obtain information on daily routines of 54 adults with ASD living in New Delhi, India, and about parent levels of stress associated with these routines during a study collected from January through June, 2013. Whether or not they attended a structured setting during the day (59% did so), adults engaged in some 20 activities both inside and outside their home. Contrary to our expectations, most adults were not « hidden » and were out in public at least on occasion. Higher functioning adults were more likely to attend a structured setting, but parents described challenging behaviors, both adult and parent preference, and lack of options as reasons that adults stayed home. The amount of time adults spent outside their home was not associated with parent reported stress, but stress was significantly higher for mothers who were employed. Most families described adaptation to caring for their adult children. A partnership with an Indian nongovernmental organization provided mechanisms to amplify our research findings, making them meaningful to our participants and others.
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9. Gentile I, Zappulo E, Bonavolta R, Maresca R, Messana T, Buonomo AR, Portella G, Sorrentino R, Settimi A, Pascotto A, Borgia G, Bravaccio C. {{Prevalence and Titre of Antibodies to Cytomegalovirus and Epstein-Barr Virus in Patients with Autism Spectrum Disorder}}. {In vivo (Athens, Greece)}. 2014 07-08;28(4):621-6.
Background/Aim: The etiology of autism spectrum disorders (ASD) is currently unknown. Few studies have explored the role of Cytomegalovirus (CMV) and Epstein Barr Virus (EBV) as potential etiological factors of ASD. The aim of the present study was to evaluate the seropositivity rate and antibody titre to CMV and EBV in children with ASD compared to same-aged healthy controls. Patients and Methods: We compared the seropositivity rate and titre of antibodies to CMV and EBV in 54 children with ASD (19 with autistic disorder and 35 with non-autistic disorder ASD) and in 46 controls. Results: Seropositivity rate and titre of the two antibodies were not dissimilar between cases and controls. However, considering only patients with ASD, those seropositive for CMV tended to test worse to the major severity scales than the seronegative ones. Conclusion: Titre and seropositivity rate of antibodies to CMV and EBV are similar between children with ASD and healthy controls.
10. Gentile I, Zappulo E, Bonavolta R, Maresca R, Riccio MP, Buonomo AR, Portella G, Settimi A, Pascotto A, Borgia G, Bravaccio C. {{Exposure to Varicella Zoster Virus Is Higher in Children with Autism Spectrum Disorder than in Healthy Controls. Results from a Case-control Study}}. {In vivo (Athens, Greece)}. 2014 07-08;28(4):627-31.
Background/Aim: Autism spectrum disorder (ASD) is a group of central nervous system disorders lacking a definite etiology. The aim of the present study was to compare the exposure rate and titer of antibodies to Varicella Zoster Virus (VZV) in children with ASD and in healthy controls. Patients and Methods: We enrolled 54 children with ASD and 46 control individuals. Results: The exposure rate and titer of anti-VZV antibodies were significantly higher in children with ASD compared to controls (59% vs. 39% and 694 mIU/ml vs. 94 mIU/ml, respectively). Conclusion: In the present case-control study, exposure to VZV was found to be independently associated with ASD.
11. Gentile I, Zappulo E, Bonavolta R, Maresca R, Riccio MP, Buonomo AR, Portella G, Vallefuoco L, Settimi A, Pascotto A, Borgia G, Bravaccio C. {{Prevalence of Herpes Simplex Virus 1 and 2 Antibodies in Patients with Autism Spectrum Disorders}}. {In vivo (Athens, Greece)}. 2014 07-08;28(4):667-71.
Background/Aim: The etiology of autism spectrum disorder (ASD) is unknown, even though it is hypothesized that a viral infection could trigger this disorder. The aim of this study was to evaluate the seropositivity rate and antibody level of Herpes Simplex Virus 1 (HSV1) and Herpes Simplex Virus 2 (HSV2) in children with ASD compared to same-aged healthy controls. Patients and Methods: We compared seropositivity rate and levels of antibodies to HSV1/2 in 54 children with ASD (19 with autistic disorder and 35 with non-autistic ASD) and in 46 controls. Results: Seropositivity rate and levels of anti-HSV1/2 were not dissimilar between cases and controls. Exposure to HSV2 was minimal. Conclusion: Rate of contact with HSV1 and HSV2 assessed by the mean of detection of specific antibodies was similar between children with ASD and healthy controls.
12. Gholizadeh S, Arsenault J, Xuan IC, Pacey LK, Hampson DR. {{Reduced Phenotypic Severity Following Adeno-Associated Virus Mediated Fmr1 Gene Delivery in Fragile X Mice}}. {Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology}. 2014 Jul 7.
Fragile X syndrome is a neurodevelopmental disorder caused by a trinucleotide repeat expansion in the FMR1 gene that codes for Fragile X Mental Retardation Protein (FMRP). To determine if FMRP expression in the central nervous system could reverse phenotypic deficits in the Fmr1 knockout mouse model of fragile X, we used a single-stranded adeno-associated viral vector (AAV) with viral capsids from serotype 9 that contained a major isoform of FMRP. FMRP transgene expression was driven by the neuron-selective synapsin-1 promoter. The vector was delivered to the brain via a single bilateral intra-cerebroventricular injection into neonatal Fmr1 knockout mice and transgene expression and behavioral assessments were conducted 22-26 and 50-56 days post-injection. Western blotting and immunocytochemical analyses of AAV-FMRP injected mice revealed FMRP expression in the striatum, hippocampus, retrosplenial cortex and cingulate cortex. Cellular expression was selective for neurons and reached approximately 50% of wild-type levels in the hippocampus and cortex at 56 days post-injection. The pathologically elevated repetitive behavior and the deficit in social dominance behavior seen in PBS-injected Fmr1 knockout mice were reversed in AAV-FMRP injected mice. These results provide the first proof-of-principle that gene therapy can correct specific behavioral abnormalities in the mouse model of fragile X syndrome.Neuropsychopharmacology accepted article preview online, 07 July 2014; doi:10.1038/npp.2014.167.
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13. Jeste SS, Wu JY, Senturk D, Varcin K, Ko J, McCarthy B, Shimizu C, Dies K, Vogel-Farley V, Sahin M, Nelson CA, 3rd. {{Early developmental trajectories associated with ASD in infants with tuberous sclerosis complex}}. {Neurology}. 2014 Jul 8;83(2):160-8.
OBJECTIVE: We performed a longitudinal cohort study of infants with tuberous sclerosis complex (TSC), with the overarching goal of defining early clinical, behavioral, and biological markers of autism spectrum disorder (ASD) in this high-risk population. METHODS: Infants with TSC and typically developing controls were recruited as early as 3 months of age and followed longitudinally until 36 months of age. Data gathered at each time point included detailed seizure history, developmental testing using the Mullen Scales of Early Learning, and social-communication assessments using the Autism Observation Scale for Infants. At 18 to 36 months, a diagnostic evaluation for ASD was performed using the Autism Diagnostic Observation Schedule. RESULTS: Infants with TSC demonstrated delays confined to nonverbal abilities, particularly in the visual domain, which then generalized to more global delays by age 9 months. Twenty-two of 40 infants with TSC were diagnosed with ASD. Both 12-month cognitive ability and developmental trajectories over the second and third years of life differentiated the groups. By 12 months of age, the ASD group demonstrated significantly greater cognitive delays and a significant decline in nonverbal IQ from 12 to 36 months. CONCLUSIONS: This prospective study characterizes early developmental markers of ASD in infants with TSC. The early delay in visual reception and fine motor ability in the TSC group as a whole, coupled with the decline in nonverbal ability in infants diagnosed with ASD, suggests a domain-specific pathway to ASD that can inform more targeted interventions for these high-risk infants.
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14. Kim SH, Kim KH, Lim YM, Moon JY, Yang WI, Kim IJ, Lim SW. {{Delayed embolisation of Amplatzer ASD closure device caused partial obstruction of left ventricular outflow tract}}. {Cardiovascular journal of Africa}. 2014;25(3):e1-3.
A 54-year-old male presented with symptoms of dyspnoea, and oedema of the lower extremities. Transthoracic echocardiography (TTE) revealed secondum-type atrial septal defect (ASD). He successfully received a 30-mm Amplatzer ASD closure device percutaneously. Echocardiography immediately after the procedure and the next day showed a wellpositioned device. He was discharged the next day on 100 mg aspirin daily and warfarinisation due to atrial fibrillation. A month later, he revisited the hospital due to recurrence of dyspnoea and a grade 2 systolic murmur was heard on the left parasternal border. A chest X-ray showed abnormal location of the closure device and TTE revealed re-appearance of the ASD and an embolised Amplatzer device in the left ventricular outflow tract (LVOT) with partial obstruction. He requested surgery to remove the Amplatzer device and received an ASD patch repair, tricuspid valve repair and modified Maze operation concurrently. He is now in routine follow up without any other complications.
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15. McGee A, Li G, Lu Z, Qiu S. {{Convergent synaptic and circuit substrates underlying autism genetic risks}}. {Frontiers in biology}. 2014 Feb 1;9(2):137-50.
There has been a surge of diagnosis of autism spectrum disorders (ASD) over the past decade. While large, high powered genome screening studies of children with ASD have identified numerous genetic risk factors, research efforts to understanding how each of these risk factors contributes to the development autism has met with limited success. Revealing the mechanisms by which these genetic risk factors affect brain development and predispose a child to autism requires mechanistic understanding of the neurobiological changes underlying this devastating group of developmental disorders at multifaceted molecular, cellular and system levels. It has been increasingly clear that the normal trajectory of neurodevelopment is compromised in autism, in multiple domains as much as aberrant neuronal production, growth, functional maturation, patterned connectivity, and balanced excitation and inhibition of brain networks. Many autism risk factors identified in humans have been now reconstituted in experimental mouse models to allow mechanistic interrogation of the biological role of the risk gene. Studies utilizing these mouse models have revealed that underlying the enormous heterogeneity of perturbed cellular events, mechanisms directing synaptic and circuit assembly may provide a unifying explanation for the pathophysiological changes and behavioral endophenotypes seen in autism, although synaptic perturbations are far from being the only alterations relevant for ASD. In this review, we discuss synaptic and circuit abnormalities obtained from several prevalent mouse models, particularly those reflecting syndromic forms of ASD that are caused by single gene perturbations. These compiled results reveal that ASD risk genes contribute to proper signaling of the developing gene networks that maintain synaptic and circuit homeostasis, which is fundamental to normal brain development.
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16. Mellios N, Woodson J, Garcia RI, Crawford B, Sharma J, Sheridan SD, Haggarty SJ, Sur M. {{beta2-Adrenergic receptor agonist ameliorates phenotypes and corrects microRNA-mediated IGF1 deficits in a mouse model of Rett syndrome}}. {Proceedings of the National Academy of Sciences of the United States of America}. 2014 Jul 8;111(27):9947-52.
Rett syndrome is a severe childhood onset neurodevelopmental disorder caused by mutations in methyl-CpG-binding protein 2 (MECP2), with known disturbances in catecholamine synthesis. Here, we show that treatment with the beta2-adrenergic receptor agonist clenbuterol increases survival, rescues abnormalities in respiratory function and social recognition, and improves motor coordination in young male Mecp2-null (Mecp2(-/y)) mice. Importantly, we demonstrate that short-term treatment with clenbuterol in older symptomatic female heterozygous (Mecp2(-/+)) mice rescues respiratory, cognitive, and motor coordination deficits, and induces an anxiolytic effect. In addition, we reveal abnormalities in a microRNA-mediated pathway, downstream of brain-derived neurotrophic factor that affects insulin-like growth factor 1 (IGF1) expression in Mecp2(-/y) mice, and show that treatment with clenbuterol restores the observed molecular alterations. Finally, cotreatment with clenbuterol and recombinant human IGF1 results in additional increases in survival in male null mice. Collectively, our data support a role for IGF1 and other growth factor deficits as an underlying mechanism of Rett syndrome and introduce beta2-adrenergic receptor agonists as potential therapeutic agents for the treatment of the disorder.
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17. Ross CA. {{Problems with autism, catatonia and schizophrenia in DSM-5}}. {Schizophrenia research}. 2014 Jul 3.
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18. van De Sande MM, van Buul VJ, Brouns FJ. {{Autism and nutrition: the role of the gut-brain axis}}. {Nutrition research reviews}. 2014 Jul 8:1-16.
Autism spectrum disorder (ASD) is characterised by deficits in the ability to socialise, communicate and use imagination, and displays of stereotypical behaviour. It is widely accepted that ASD involves a disorder in brain development. However, the real causes of the neurodevelopmental disorders associated with ASD are not clear. In this respect, it has been found that a majority of children with ASD display gastrointestinal symptoms, and an increased intestinal permeability. Moreover, large differences in microbiotic composition between ASD patients and controls have been reported. Therefore, nutrition-related factors have been hypothesised to play a causal role in the aetiology of ASD and its symptoms. Through a review of the literature, it was found that abnormalities in carbohydrate digestion and absorption could explain some of the gastrointestinal problems observed in a subset of ASD patients, although their role in the neurological and behavioural problems remains uncertain. In addition, the relationship between an improved gut health and a reduction of symptoms in some patients was evaluated. Recent trials involving gluten-free diets, casein-free diets, and pre- and probiotic, and multivitamin supplementation show contradictive but promising results. It can be concluded that nutrition and other environmental influences might trigger an unstable base of genetic predisposition, which may lead to the development of autism, at least in a subset of ASD patients. Clear directions for further research to improve diagnosis and treatment for the different subsets of the disorder are provided.
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19. Vivanti G, Prior M, Williams K, Dissanayake C. {{Predictors of outcomes in autism early intervention: why don’t we know more?}}. {Frontiers in pediatrics}. 2014;2:58.
Response to early intervention programs in autism is variable. However, the factors associated with positive versus poor treatment outcomes remain unknown. Hence the issue of which intervention/s should be chosen for an individual child remains a common dilemma. We argue that lack of knowledge on « what works for whom and why » in autism reflects a number of issues in current approaches to outcomes research, and we provide recommendations to address these limitations. These include: a theory-driven selection of putative predictors; the inclusion of proximal measures that are directly relevant to the learning mechanisms demanded by the specific educational strategies; the consideration of family characteristics. Moreover, all data on associations between predictor and outcome variables should be reported in treatment studies.
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20. Weiss AL, Rohland P. {{« Measuring up » to ethical standards in service delivery to college students on the Autism Spectrum: A practical application of Powell’s model for ethical practices in clinical phonetics and linguistics}}. {Clinical linguistics & phonetics}. 2014 Jul;28(7-8):627-38.
Abstract This paper examined an interdisciplinary college-based support programme, the Communication Coaching Program (CCP), designed for students diagnosed on the autism spectrum in light of six ethical constructs described by Powell. Collecting data to monitor the successes and ongoing needs of individual participants in the programme is of vital importance, of course, but only addresses a portion of the efficacy question. In addition, the authors, who co-direct the programme and represent different professional expertise and perspectives, recognize the importance of determining whether their evolving intervention model has also been successful in meeting the ethical standards of their respective professions. Careful review of the 4 years of the CCP’s operation in terms of ethical constructs has yielded evidence that the CCP, although based on sound principles of theory and scholarship, should be further individualized to meet the particular needs of participants diagnosed with deficits in social communication and executive functioning skills.
