1. Bass MM, Duchowny CA, Llabre MM. {{The Effect of Therapeutic Horseback Riding on Social Functioning in Children with Autism}}. {J Autism Dev Disord};2009 (Apr 7)
This study evaluated the effects of therapeutic horseback riding on social functioning in children with autism. We hypothesized that participants in the experimental condition (n = 19), compared to those on the wait-list control (n = 15), would demonstrate significant improvement in social functioning following a 12-weeks horseback riding intervention. Autistic children exposed to therapeutic horseback riding exhibited greater sensory seeking, sensory sensitivity, social motivation, and less inattention, distractibility, and sedentary behaviors. The results provide evidence that therapeutic horseback riding may be a viable therapeutic option in treating children with autism spectrum disorders.
2. Hughes V. {{Blueprint for autism research put forward}}. {Nat Med};2009 (Apr);15(4):349.
3. Jyonouchi H. {{Food allergy and autism spectrum disorders: is there a link?}} {Curr Allergy Asthma Rep};2009 (May);9(3):194-201.
Gastrointestinal (GI) symptoms are common comorbidities in children with autism spectrum disorders (ASDs). Parents often attribute these GI symptoms to food allergy (FA), although an evaluation for IgE-mediated FA is often unrevealing. Our previous studies indicated a high prevalence of non-IgE-mediated FA in young children with ASDs. Therefore, non-IgE-mediated FA may account for some but not all GI symptoms observed in children with ASDs. This raises the question of what treatment measures are applicable to ASD children with GI symptoms. A wide variety of dietary supplements and dietary intervention measures for ASD children have been promoted by medical professionals practicing complementary and alternative medicine despite the lack of rigorous scientific validation in most instances. This review summarizes possible (or proposed) etiologies of GI symptoms in ASD children and discusses risks and possible benefits of intervention measures promoted by complementary and alternative practitioners, with emphasis on FA.
4. Kumar RA, Christian SL. {{Genetics of autism spectrum disorders}}. {Curr Neurol Neurosci Rep};2009 (May);9(3):188-197.
Autism spectrum disorders (ASDs) are a clinically complex group of childhood disorders that have firm evidence of an underlying genetic etiology. Many techniques have been used to characterize the genetic bases of ASDs. Linkage studies have identified several replicated susceptibility loci, including 2q24-2q31, 7q, and 17q11-17q21. Association studies and mutation analysis of candidate genes have implicated the synaptic genes NRXN1, NLGN3, NLGN4, SHANK3, and CNTNAP2 in ASDs. Traditional cytogenetic approaches highlight the high frequency of large chromosomal abnormalities (3%-7% of patients), including the most frequently observed maternal 15q11-13 duplications (1%-3% of patients). Newly developed techniques include high-resolution DNA microarray technologies, which have discovered formerly undetectable submicroscopic copy number variants, and genomewide association studies, which allow simultaneous detection of multiple genes associated with ASDs. Although great progress has been made in autism genetics, the molecular bases of most ASDs remains enigmatic.
5. Lind SE, Bowler DM. {{Recognition Memory, Self-Other Source Memory, and Theory-of-Mind in Children with Autism Spectrum Disorder}}. {J Autism Dev Disord};2009 (Apr 8)
This study investigated semantic and episodic memory in autism spectrum disorder (ASD), using a task which assessed recognition and self-other source memory. Children with ASD showed undiminished recognition memory but significantly diminished source memory, relative to age- and verbal ability-matched comparison children. Both children with and without ASD showed an « enactment effect », demonstrating significantly better recognition and source memory for self-performed actions than other-person-performed actions. Within the comparison group, theory-of-mind (ToM) task performance was significantly correlated with source memory, specifically for other-person-performed actions (after statistically controlling for verbal ability). Within the ASD group, ToM task performance was not significantly correlated with source memory (after controlling for verbal ability). Possible explanations for these relations between source memory and ToM are considered.
6. Russo N, Zecker S, Trommer B, Chen J, Kraus N. {{Effects of Background Noise on Cortical Encoding of Speech in Autism Spectrum Disorders}}. {J Autism Dev Disord};2009 (Apr 8)
This study provides new evidence of deficient auditory cortical processing of speech in noise in autism spectrum disorders (ASD). Speech-evoked responses (~100-300 ms) in quiet and background noise were evaluated in typically-developing (TD) children and children with ASD. ASD responses showed delayed timing (both conditions) and reduced amplitudes (quiet) compared to TD responses. As expected, TD responses in noise were delayed and reduced compared to quiet responses. However, minimal quiet-to-noise response differences were found in children with ASD, presumably because quiet responses were already severely degraded. Moreover, ASD quiet responses resembled TD noise responses, implying that children with ASD process speech in quiet only as well as TD children do in background noise.
7. Zeev BB, Bebbington A, Ho G, Leonard H, de Klerk N, Gak E, Vecksler M, Christodoulou J. {{The common BDNF polymorphism may be a modifier of disease severity in Rett syndrome}}. {Neurology};2009 (Apr 7);72(14):1242-1247.
BACKGROUND: Rett syndrome (RTT) is caused by mutations in the transcriptional repressor methyl CpG-binding protein 2 (MECP2). Brain-derived neurotrophic factor (BDNF) is a neurotrophic factor playing a major role in neuronal survival, neurogenesis, and plasticity, and it has been shown that BDNF expression is regulated by MeCP2 through a complex interaction. A common polymorphism of BDNF (Val66Met [p.V66M]) has been found to correlate with severity and course of several neuropsychiatric disorders. METHODS: We examined the association between disease severity score, assessed by the modified Percy score, and BDNF polymorphism, using regression methods, in 125 mutation-positive patients with RTT from the Australian Rett Syndrome Database and an Israeli cohort. RESULTS: Those who were heterozygous (Val/Met) had slightly more severe disease than those who were homozygous for the wild-type (Val/Val) BDNF polymorphism (increased severity score 2.1, p = 0.09). In those with p.R168X, a commonly occurring MECP2 mutation in RTT, there was a 6-point increase in severity score for those who were heterozygous for the BDNF polymorphism, both unadjusted (p = 0.02) and adjusted for age (p = 0.03). Individuals with the p.R168X mutation and heterozygous for the BDNF polymorphism were also at an increased risk of seizure onset (hazard ratio 5.3, 95% confidence interval 1.6-17.7) compared with those homozygous for the wild-type BDNF allele. CONCLUSIONS: In addition to mutation type and degree of X-chromosome skewing, the common brain-derived neurotrophic factor (BDNF) polymorphism appears to be another genetic modifier of Rett syndrome (RTT) severity. This suggests that BDNF function may play a significant role in the pathogenesis of RTT.
