We find compelling support for a polygenic cause of ASD, with at least part of the inheritance attributable to variations at one or more genes. The data are consistent with recent theoretical and experimental models that postulate developmental disorders may result from altered levels or patterning in key gene regulatory networks during fetal development. Furthermore, our findings suggest the discovery of novel candidate genes for ASD.
Autism is a genetically heterogenous syndrome that encompasses a wide spectrum of disorders and behaviors; moreover, these disorders are often comorbid. The spectrum seems to include autism itself, as well as pervasive developmental disorder with or without autism. It is a critical question how best to diagnose autism.
The common signs of autism spectrum disorder include social and communication impairments, behaviours such as repetitive behaviours or repetitive movements, social avoidance and low interest or engagement in certain activities. However, these can manifest in a variety of ways. It appears children with autism spectrum disorder develop their signs of autism spectrum disorder between the ages of 15 and 24 months.\n
Results from a recent clinical trial shows that the annual incidence of ASD and PDD is probably underestimated because of the inclusion of individuals meeting DSM-IV criteria for ASD that had no previous or recent contact with a professional, but who may be misdiagnosed with ASD because of lack of mental illnesses. Further systematic efforts are necessary to ascertain more accurate data about ASD.
Recent findings, and recommendations, are discussed in the context of a current framework for understanding causation in autism spectrum disorder. This framework emphasizes the role of genes and epigenetic modification, neurotransmitter dysregulation, altered developmental processes, and immune dysregulation as pathways through which environmental factors, such as infections and environmental toxins, can exacerbate ASD symptomology in affected individuals through mechanisms that do not involve genetic mutations.
The evidence-based literature on ASD diagnosis and treatment is limited. There are limited data on the efficacy of treatment of ASD. Findings support the idea that ASD can often be controlled with effective intervention, and that ASD is a challenging condition with potential for cure (though limited and incomplete evidence indicates that the ASD disability phenotype can be less strongly correlated with neurodevelopmental outcome after intervention than in the case of neurodevelopmental disorders caused by a non-genetic etiology).
The findings contribute to the growing literature and demonstrate that clinicians need to be trained across all three domains of emotion learning in order to deliver effective emotional and interpersonal interventions. In particular, the findings suggest that clinicians need to train not only in emotion recognition but also in understanding emotion-laden social interaction in order to facilitate effective therapeutic outcomes. As such, training clinicians to understand emotion-laden situations within the context of the social relationships (that is, the dynamic dimension) of interpersonal relationships is likely to lead to better outcomes, both for the client and for the clinician.
There appears to be a trend towards greater understanding of ASD treatment over the past decade. There is a wide range of treatments available to patients with ASD and many parents are not aware of the possible options.
In this population, TINE seems to be effective both as the modality of training (i.e. alone or in combination with other treatments) and across the contexts of therapy (i.e. one-off, once or twice weekly.) However, the addition of TINE to the regular care did not appear to improve outcomes, and may even lead to poorer care experiences. Results from a recent clinical trial need to be interpreted in light of the absence of effect sizes greater than d=.05 for TINE when used by therapists/educators.
Although ASD may represent a genetic etiological basis for certain symptom dimensions, it does not appear to run in families. Clinicians and researchers need to be aware of possible false-positive findings in ASD families.
Data from a recent study is the first to provide rigorous data on the effectiveness of TINE and suggests that TINE is both effective and practical for the large-group dynamics contexts it is designed for. Data from a recent study support the further development, refinement, and refinement of TINE, with the goal of generalizing TINE to other contexts, while also working closely to improve the TINE training process.
The present-day research focus is focused on determining the genes and proteins that are mutated in autism spectrum disorder, and to find a cure. Genetic testing is now available to screen for mutations of genes in the autism spectrum. Clinical trials of gene therapy have shown positive results. Research and clinical trials are being conducted for potential use of fetal cell therapy and epigenetic therapy in autism spectrum disorder.