The purpose of this study is to determine the effects of fever on the behavior of young children (aged 2 to 7 years) with autism spectrum disorder (ASD), compared with a typically developing control group. Although clinical case reports have described behavioral changes in response to fever in children with ASD, few empirical investigations of this phenomenon have been conducted.
An imbalance in excitatory/inhibitory transmission, due to alterations in GABAergic signaling, has been suggested as an underlying cause of autism. These studies argue that the GABAergic system represents a viable therapeutic target for autism. Indeed, the GABA-B receptor agonist R-baclofen has been shown to ameliorate social deficits and repetitive behaviors in two mouse models of autism1. However, baclofen is known to exhibit relatively poor blood-brain-barrier permeability, arguing for the development of drug treatments more accessible to the central nervous system. Yet such drug discovery efforts are complicated by a lack of suitable radiotracers for imaging GABA-B receptors.
Social recognition is essential for individuals to survive, reproduce and raise their young. In people, social recognition can be severely affected by conditions such as autism spectrum disorders (ASDs). Interestingly, anecdotal reports from parents and professional caregivers suggest that children with ASD can exhibit improved social interactions during episodes of fever. Deciphering the unique characteristics of social recognition in animals and people, and understanding how this behavior may be affected by external influences, are critical steps toward helping to treat individuals suffering from social behavior deficits.
Autism spectrum disorders (ASDs) are heterogeneous neurodevelopmental syndromes characterized by repetitive behaviors and deficits in language development and social interactions. To understand how ASDs affect behaviors in people, genetic models of ASDs in laboratory mice are needed; such models will allow researchers to test theories about how ASDs affect the brain and lead to behavioral symptoms, and will enable tests of future drugs to treat ASDs.
Autism spectrum disorder (ASD), affecting 1 in 68 children in the U.S., is a significant unresolved public health concern. The clinical presentations of ASD can be quite broad, and recent evidence points to many different genetic causes. This heterogeneity could lead to a scientific and clinical impasse; each cause of ASD has its own disrupted mechanisms and requires its own unique treatment. However, a more optimistic interpretation, for which there is now accumulating evidence, is that many different primary causes of ASD actually converge on a limited subset of biochemical pathways in nerve cells that mediate cell growth and function. Demonstrating that such a mechanistic convergence exists would be a significant step forward for the field.
Recent advances in genome-wide approaches for gene discovery in autism spectrum disorders (ASDs) have identified a large list of strongly associated ASD risk genes, as well as an even larger list of potential ASD risk genes. In total, these comprise approximately 250 genes. In order to further distinguish the true ASD risk genes from false-positive associations, additional sequencing data is required. Molecular inversion probe (MIP) sequencing is an efficient approach because of the low cost, potential for parallelization and high-throughput capacity.
Chromosomal microarray analysis (CMA) is a robust technology officially recommended for children with autism spectrum disorders (ASDs). However, CMA genetic testing might raise ethical, legal and social issues such as stigmatization, health insurance concerns and test misconceptions. Therefore, it is essential to understand what might motivate or inhibit test decisions among parents of children with ASD.
Sensitive, standardized, reliable measures of outcomes for clinical trials attempting to change behavior and function in children and adults with autism spectrum disorder (ASD) have been extremely limited to date. Previous clinical trials have often relied on a single measure to quantify change, determined change in one domain or context (i.e., language or solely parent report or assessments only in the clinic), or used an approach measure with limited capability for replication, thus reducing the scope of the research.
Autism spectrum disorders (ASD) are strongly sex-biased. Boys are four times more likely to receive a diagnosis than girls, with ASDs affecting an estimated 1 in 42 males in the U.S. The biological mechanisms contributing to these sex differences are currently unknown.
Research assessing the effectiveness of treatments in autism spectrum disorder (ASD) is limited by a lack of scalable and quantifiable autism-specific treatment response measures. Assessing treatment success would be benefited by the development of response measures that can be administered ‘blindly’ and are sensitive enough to capture change over short periods of time, flexible enough to be used across studies and are standardized in order to be comparable across sites.