1. Curran J. {{‘I move therefore I am’: The anoetic ideomotor theory of autism}}. {Aust N Z J Psychiatry}. 2014.
Lien vers le texte intégral (Open Access ou abonnement)
2. Engineer CT, Centanni TM, Im KW, Kilgard MP. {{Speech sound discrimination training improves auditory cortex responses in a rat model of autism}}. {Front Syst Neurosci}. 2014; 8: 137.
Children with autism often have language impairments and degraded cortical responses to speech. Extensive behavioral interventions can improve language outcomes and cortical responses. Prenatal exposure to the antiepileptic drug valproic acid (VPA) increases the risk for autism and language impairment. Prenatal exposure to VPA also causes weaker and delayed auditory cortex responses in rats. In this study, we document speech sound discrimination ability in VPA exposed rats and document the effect of extensive speech training on auditory cortex responses. VPA exposed rats were significantly impaired at consonant, but not vowel, discrimination. Extensive speech training resulted in both stronger and faster anterior auditory field (AAF) responses compared to untrained VPA exposed rats, and restored responses to control levels. This neural response improvement generalized to non-trained sounds. The rodent VPA model of autism may be used to improve the understanding of speech processing in autism and contribute to improving language outcomes.
Lien vers le texte intégral (Open Access ou abonnement)
3. Isshiki M, Tanaka S, Kuriu T, Tabuchi K, Takumi T, Okabe S. {{Enhanced synapse remodelling as a common phenotype in mouse models of autism}}. {Nat Commun}. 2014; 5: 4742.
Developmental deficits in neuronal connectivity are considered to be present in patients with autism spectrum disorders (ASDs). Here we examine this possibility by using in vivo spine imaging in the early postnatal cortex of ASD mouse models. Spines are classified by the presence of either the excitatory postsynaptic marker PSD-95 or the inhibitory postsynaptic marker gephyrin. ASD mouse models show consistent upregulation in the dynamics of PSD-95-positive spines, which may subsequently contribute to stable synaptic connectivity. In contrast, spines receiving inputs from the thalamus, detected by the presence of gephyrin clusters, are larger, highly stable and unaffected in ASD mouse models. Importantly, two distinct mouse models, human 15q11-13 duplication and neuroligin-3 R451C point mutation, show highly similar phenotypes in spine dynamics. This selective impairment in dynamics of PSD-95-positive spines receiving intracortical projections may be a core component of early pathological changes and be a potential target of early intervention.
Lien vers le texte intégral (Open Access ou abonnement)
4. James WH. {{An update on the hypothesis that one cause of autism is high intrauterine levels of testosterone of maternal origin}}. {J Theor Biol}. 2014; 355: 33-9.
Baron-Cohen’s hypothesis that autism is caused by exposure to high intrauterine testosterone levels is considered in the context of (1) my hormonal hypothesis of sex ratio and (2) the notion of multifactorial inheritance. This yields the suggestions that (1) female cases of autism may be the product of (high genetic loading+moderate environmental exposure) and male cases of (high environmental exposure+moderate genetic loading), (2) one environmental agent is intrauterine testosterone and (3) the mother is the major source of that testosterone. These suggestions may help to explain most of the major established epidemiological risk factors for autism. These include various forms of pathology associated with psychological and/or physical stress. Stress of many sorts promotes the secretion of adrenal androgens in women. The three suggestions above may also explain some recently described features of autism including the psychological, behavioural and neuroanatomical differences between male and female cases.
Lien vers le texte intégral (Open Access ou abonnement)
5. Nair MK, Russell PS, George B, Prasanna GL, Bhaskaran D, Leena ML, Russell S, Mammen P. {{CDC Kerala 9: Effectiveness of Low Intensity Home Based Early Intervention for Autism Spectrum Disorder in India}}. {Indian J Pediatr}. 2014.
OBJECTIVE: To validate effectiveness of low intensity, home based early intervention (EI) models in autism for countries with low disability resources. METHODS: Fifty-two toddlers and young children were assessed before and after intervention with Childhood Autism Rating Scale, Vineland Social Maturity Scale, and Receptive-Expressive Emergent Language Scale. Developmental and speech therapists helped mothers assemble low-cost training kits based on the developmental age of the child, gave initial training in the basic behavioral technique to address the three autism symptom clusters at home. Follow-up support was given either on a weekly, fortnightly or monthly basis. Most of the children were also placed in play-schools. Data was analyzed using appropriate bivariate and multivariate techniques. RESULTS: There was statistical and clinical amelioration in the severity of autism, with acquisition of social skills and language skills (all P = 0.001) after intervention in children with mild to severe autism. Gender showed a trend in becoming a significant predictor for intervention response. CONCLUSIONS: Low-intensity, home-based EI can be effectively used in situations where there is paucity of disability resources in countries like India, especially in primary-care and community settings.
Lien vers le texte intégral (Open Access ou abonnement)
6. Righi G, Tierney AL, Tager-Flusberg H, Nelson CA. {{Functional connectivity in the first year of life in infants at risk for autism spectrum disorder: an EEG study}}. {PLoS One}. 2014; 9(8): e105176.
In the field of autism research, recent work has been devoted to studying both behavioral and neural markers that may aide in early identification of autism spectrum disorder (ASD). These studies have often tested infants who have a significant family history of autism spectrum disorder, given the increased prevalence observed among such infants. In the present study we tested infants at high- and low-risk for ASD (based on having an older sibling diagnosed with the disorder or not) at 6- and 12-months-of-age. We computed intrahemispheric linear coherence between anterior and posterior sites as a measure of neural functional connectivity derived from electroencephalography while the infants were listening to speech sounds. We found that by 12-months-of-age infants at risk for ASD showed reduced functional connectivity compared to low risk infants. Moreover, by 12-months-of-age infants later diagnosed with ASD showed reduced functional connectivity, compared to both infants at low risk for the disorder and infants at high risk who were not later diagnosed with ASD. Significant differences in functional connectivity were also found between low-risk infants and high-risk infants who did not go onto develop ASD. These results demonstrate that reduced functional connectivity appears to be related to genetic vulnerability for ASD. Moreover, they provide further evidence that ASD is broadly characterized by differences in neural integration that emerge during the first year of life.
Lien vers le texte intégral (Open Access ou abonnement)
7. Sundquist J, Sundquist K, Ji J. {{Autism and attention-deficit/hyperactivity disorder among individuals with a family history of alcohol use disorders}}. {Elife}. 2014; 3: e02917.
Recent studies suggest de novo mutations may involve the pathogenesis of autism and attention-deficit/hyperactivity disorder (ADHD). Based on the evidence that excessive alcohol consumption may be associated with an increased rate of de novo mutations in germ cells (sperms or eggs), we examine here whether the risks of autism and ADHD are increased among individuals with a family history of alcohol use disorders (AUDs). The standardized incidence ratios (SIRs) of autism and ADHD among individuals with a biological parental history of AUDs were 1.39 (95% CI 1.34-1.44) and 2.19 (95% CI 2.15-2.23), respectively, compared to individuals without an affected parent. Among offspring whose parents were diagnosed with AUDs before their birth, the corresponding risks were 1.46 (95% CI 1.36-1.58) and 2.70 (95% CI 2.59-2.81), respectively. Our study calls for extra surveillance for children with a family history of AUDs, and further studies examining the underlying mechanisms are needed.DOI: http://dx.doi.org/10.7554/eLife.02917.001.
