1. Aziz A, Harrop SP, Bishop NE. {{Characterization of the deleted in autism 1 protein family: implications for studying cognitive disorders}}. {PLoS One};2011;6(1):e14547.
Autism spectrum disorders (ASDs) are a group of commonly occurring, highly-heritable developmental disabilities. Human genes c3orf58 or Deleted In Autism-1 (DIA1) and cXorf36 or Deleted in Autism-1 Related (DIA1R) are implicated in ASD and mental retardation. Both gene products encode signal peptides for targeting to the secretory pathway. As evolutionary medicine has emerged as a key tool for understanding increasing numbers of human diseases, we have used an evolutionary approach to study DIA1 and DIA1R. We found DIA1 conserved from cnidarians to humans, indicating DIA1 evolution coincided with the development of the first primitive synapses. Nematodes lack a DIA1 homologue, indicating Caenorhabditis elegans is not suitable for studying all aspects of ASD etiology, while zebrafish encode two DIA1 paralogues. By contrast to DIA1, DIA1R was found exclusively in vertebrates, with an origin coinciding with the whole-genome duplication events occurring early in the vertebrate lineage, and the evolution of the more complex vertebrate nervous system. Strikingly, DIA1R was present in schooling fish but absent in fish that have adopted a more solitary lifestyle. An additional DIA1-related gene we named DIA1-Like (DIA1L), lacks a signal peptide and is restricted to the genomes of the echinoderm Strongylocentrotus purpuratus and cephalochordate Branchiostoma floridae. Evidence for remarkable DIA1L gene expansion was found in B. floridae. Amino acid alignments of DIA1 family gene products revealed a potential Golgi-retention motif and a number of conserved motifs with unknown function. Furthermore, a glycine and three cysteine residues were absolutely conserved in all DIA1-family proteins, indicating a critical role in protein structure and/or function. We have therefore identified a new metazoan protein family, the DIA1-family, and understanding the biological roles of DIA1-family members will have implications for our understanding of autism and mental retardation.
2. Barnes VM. {{Dentistry and autism}}. {J Am Dent Assoc};2011 (Feb);142(2):126.
3. Jackett JM. {{Transition and beyond for individuals with autism spectrum disorders (ASD): a New Jersey case study of the adult service sector, its inherent shortcomings, and hope for the future}}. {Seton Hall Law Rev};2010;40(4):1733-1774.
4. MacFabe DF, Cain NE, Boon F, Ossenkopp KP, Cain DP. {{Effects of the enteric bacterial metabolic product propionic acid on object-directed behavior, social behavior, cognition, and neuroinflammation in adolescent rats: Relevance to autism spectrum disorder}}. {Behav Brain Res};2011 (Feb 2);217(1):47-54.
Recent evidence suggests that a variety of environmental factors, including dietary and gastrointestinal agents, may contribute to autism spectrum disorders (ASD). Here we administered propionic acid (PPA), a short chain fatty acid that is used as a food preservative and also is a metabolic end-product of enteric bacteria in the gut, to adolescent (41 +/- 4 days) male rats in a study of restricted/repetitive behavior, social behavior, and cognition. The goal was to further evaluate the effects of PPA in young rodents. PPA (4 mul of 0.26 M solution) was administered intracerebroventricularly prior to each behavioral test. Rats treated with PPA displayed restricted behavioral interest to a specific object among a group of objects, impaired social behavior, and impaired reversal in a T-maze task compared to controls given phosphate buffered saline. Immunohistochemical analysis of brain tissue from PPA rats revealed reactive astrogliosis and activated microglia, indicating an innate neuroinflammatory response. These findings are consistent with our earlier findings of ASD-relevant behavioral and brain events in adult rats given PPA, and support further study of effects of PPA in young rodents by establishing similar effects in adolescent animals.
5. Moran JM, Young LL, Saxe R, Lee SM, O’Young D, Mavros PL, Gabrieli JD. {{Impaired theory of mind for moral judgment in high-functioning autism}}. {Proc Natl Acad Sci U S A};2011 (Jan 31)
High-functioning autism (ASD) is characterized by real-life difficulties in social interaction; however, these individuals often succeed on laboratory tests that require an understanding of another person’s beliefs and intentions. This paradox suggests a theory of mind (ToM) deficit in adults with ASD that has yet to be demonstrated in an experimental task eliciting ToM judgments. We tested whether ASD adults would show atypical moral judgments when they need to consider both the intentions (based on ToM) and outcomes of a person’s actions. In experiment 1, ASD and neurotypical (NT) participants performed a ToM task designed to test false belief understanding. In experiment 2, the same ASD participants and a new group of NT participants judged the moral permissibility of actions, in a 2 (intention: neutral/negative) x 2 (outcome: neutral/negative) design. Though there was no difference between groups on the false belief task, there was a selective difference in the moral judgment task for judgments of accidental harms, but not neutral acts, attempted harms, or intentional harms. Unlike the NT group, which judged accidental harms less morally wrong than attempted harms, the ASD group did not reliably judge accidental and attempted harms as morally different. In judging accidental harms, ASD participants appeared to show an underreliance on information about a person’s innocent intention and, as a direct result, an overreliance on the action’s negative outcome. These findings reveal impairments in integrating mental state information (e.g., beliefs, intentions) for moral judgment.
6. Nazeer A. {{Psychopharmacology of autistic spectrum disorders in children and adolescents}}. {Pediatr Clin North Am};2011 (Feb);58(1):85-97.
This article provides an overview of the psychopharmacologic management of irritability, hyperactivity, and repetitive behaviors in children and adolescents with autism spectrum disorder. A review of the current literature on medications used to treat these conditions with emphasis on randomized controlled trials is presented.
7. Trembath D. {{Book Review Editor: Rachel Mayes Autism Spectrum Disorders and AAC. Pat Mirenda & Teresa Iacono (Eds.) Baltimore, MD : Brookes . 2009 . 504 pp. US$49.95 . ISBN: 978-1-55766-953-7}}. {J Intellect Dev Disabil};2011 (Feb 1)
8. Trottier N, Kamp L, Mirenda P. {{Effects of Peer-Mediated Instruction to Teach Use of Speech-Generating Devices to Students with Autism in Social Game Routines}}. {Augment Altern Commun};2011 (Feb 2)
Supporting social interactions between students with autism spectrum disorders (ASDs) and their typically developing peers presents many challenges. The purpose of this study was to investigate the effects of a peer-mediated intervention designed to teach two students with ASD to use speech-generating devices (SGDs) to engage in interactions with peers in a social context at school. Six peer confederates (three from each student with ASD’s general education classroom) were taught to support SGD use during game activities. A multiple baseline design was used to examine the relationship between peer-mediated instruction and an increase in total communicative acts (CAs) by the two students with ASD. Results provide evidence that the confederates acquired the skills needed to support SGD use by students with ASD. The results also suggest that the intervention was effective at increasing total appropriate CAs by students with ASD. In addition, social validity ratings by all of the confederates were positive. Results are discussed regarding educational implications, limitations, and future research.
9. Yang HH, Savostyanov AN, Tsai AC, Liou M. {{Face Recognition in Asperger Syndrome: A Study on EEG Spectral Power Changes}}. {Neurosci Lett};2011 (Jan 28)
EEG reactions in emotional face recognition were studied in five participants with Asperger syndrome (AS) and seven control subjects. Control subjects showed a spectral power increase following the stimulus onset in two time-frequency intervals-(1) 150-300ms in the 1-16Hz frequency range, and (2) 300-650ms in the 1-8Hz range. Also, alpha/beta desynchronization occurred 400-1000ms after the stimulus onset with maximal amplitude in the posterior region. Theta synchronization (4-8Hz) was weaker in the AS group than in the control group, but beta2 desynchronization was stronger in the AS group. The results were interpreted in terms of automatic and voluntary control of perception.
