1. Aman MG, Arnold LE, Hollway JA. {{Assessing change in core autism symptoms: challenges for pharmacological studies}}. {J Child Adolesc Psychopharmacol};2015 (May);25(4):282-285.
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2. Barad DH, Kushnir VA, Albertini D, Gleicher N. {{CDC analysis of ICSI/autism: association is not causation}}. {Hum Reprod};2015 (May 13)
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3. Cheuk S, Lashewicz B. {{How are they doing? Listening as fathers of children with autism spectrum disorder compare themselves to fathers of children who are typically developing}}. {Autism};2015 (May 14)
The growing prevalence of autism spectrum disorder is accompanied by ongoing efforts to understand and support parents in the face of challenges related to their child’s autism spectrum disorder. Although fathers are increasingly hands-on in raising children, research focus on parenting children with autism spectrum disorder continues to be skewed toward experiences of mothers. Our purpose in this article is to contribute understandings of how fathers of children with autism spectrum disorder perceive themselves to be managing, and we undertake this by examining comparisons fathers of children with autism spectrum disorder make between their parenting experiences and experiences of fathers of typically developing children. A purposive sample of 28 fathers of children (aged 2-13 years) with autism spectrum disorder living in an urban center in Western Canada participated in in-depth interviews about their parenting successes and challenges. We found fathers speak of universal fathering experiences yet articulate their own sense of loss and efforts to come to terms with unanticipated demands associated with autism spectrum disorder. Fathers of children with autism spectrum disorder feel « pangs of jealousy » toward fathers of typically developing children, yet they are keenly attentive to their own child’s development and convey a sense of gratitude for their child’s capabilities and personality amidst an appreciation for trials and triumphs of fathering in general and fathering a child with autism spectrum disorder in particular.
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4. Helverschou SB, Rasmussen K, Steindal K, Sondanaa E, Nilsson B, Nottestad JA. {{Offending profiles of individuals with autism spectrum disorder: A study of all individuals with autism spectrum disorder examined by the forensic psychiatric service in Norway between 2000 and 2010}}. {Autism};2015 (May 14)
This study examined the characteristics of adults with autism spectrum disorder who have undergone a forensic examination and explored any relationships between the diagnosis and the offence. The reports described 41 men and 7 women. The autism spectrum disorder was diagnosed late (mean age: 25.3 years), and 22 of the 48 cases were diagnosed with autism spectrum disorder for the first time by the forensic experts. The education level and employment status were low. Family networks were close, but social networks outside the family were limited. Co-morbid diagnoses were common, and more than half of the group knew their victims. The examined individuals constitute a vulnerable and heterogeneous group, as do offenders within other diagnostic categories. Unlike most others who commit criminal acts, the majority of the individuals with autism spectrum disorder in this study showed no evidence of substance abuse, had a close relationship to their victims and were willing to confess to the accused crime. No clear association between the characteristics of autism spectrum disorder and the criminal act were identified, but in most cases, autism spectrum disorder characteristics, such as idiosyncratic comprehensions and obsessions appeared to be related to the motive for the offence.
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5. Kissin DM, Zhang Y, Boulet SL, Fountain C, Bearman P, Schieve L, Yeargin-Allsopp M, Jamieson DJ. {{Reply: CDC analysis of ICSI/autism: association is not causation}}. {Hum Reprod};2015 (May 13)
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6. Little LM, Ausderau K, Sideris J, Baranek GT. {{Activity Participation and Sensory Features Among Children with Autism Spectrum Disorders}}. {J Autism Dev Disord};2015 (May 15)
Sensory features are highly prevalent among children with autism spectrum disorders (ASD) and have been shown to cluster into four patterns of response, including hyperresponsiveness, hyporesponsiveness, enhanced perception, and sensory interests, repetitions and seeking behaviors. Given the lack of large-scale research on the differential effects of sensory response patterns on children’s participation in specific activities, this study investigated the extent to which sensory response patterns impacted six dimensions of children’s activity participation as measured by the Home and Community Activities Scale among a large, national sample of school aged children with ASD (n = 674). Using mixed model regression, results showed that sensory response patterns differentially impacted dimensions of activity participation, and associations were moderated by a number of child characteristics.
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7. Luschekina EA, Strelets VB. {{[Autism spectrum disorder. Contemporary experimental researches review]}}. {Zh Vyssh Nerv Deiat Im I P Pavlova};2014 (Nov-Dec);64(6):585-599.
Autism, like schizophrenia, are heterogeneous diseases, which are directed by both genetic factors and external influences in the early stages of development. Knowledge about the similarities and differences of these disorders can help early diagnosis and treatment. Patients with autism have specific cognitive difficulties in social relations. They are characterized by impairment of social interaction, communication and behavioral flexibility. The severity of the delay the development of autistic children, clinical and psychological indicators is correlated with an increase in the high frequency of spontaneous EEG activity. Cognitive task in autistic children, unlike normal persons, does not lead to a significant restructuring of high-frequency EEG activity, which may be a violation of the reaction mechanism to external stimuli and behavioral disorders. Abnormality in high-frequency components of EEG reactivity on cognitive task, the perception of human faces and visual illusions as well as the inadequate system of mirror neurons, can be considered common mechanisms underlying disorders of autism and schizophrenia. These general mechanisms may be considered as related to violation of the inhibition-exitation balance, controlled via GABA-transmission and NMDA-receptors. A multidimensional study of patterns of disontogenesis in autism, in addition to detailing the clinical picture of disease and rehabilitation activities, allows us to clear the fundamental understanding of the brain.
8. Tanabe Y, Fujita-Jimbo E, Momoi MY, Momoi T. {{CASPR2 forms a complex with GPR37 via MUPP1 but not with GPR37(R558Q), an autism spectrum disorder-related mutation}}. {J Neurochem};2015 (May 13)
Autism spectrum disorder (ASD) is a developmental brain disorder. Mutations in synaptic components including synaptic adhesion molecules have been found in ASD patients. Contactin-associated protein-like 2 (CASPR2) is one of the synaptic adhesion molecules associated with ASD. CASPR2 forms a complex with receptors via interaction with multiple PDZ domain protein 1 (MUPP1). Little is known about the relationship between impaired CASPR2-MUPP1-receptor complex and the pathogenesis of ASD. GPR37 is a receptor for survival factors. We recently identified mutations including R558Q in the G-protein-coupled receptor 37 (GPR37) gene in ASD patients. The mutated GPR37s accumulate in the ER. In the present study, we show that GPR37 is a component of the CASPR2-MUPP1 receptor complex in the mouse brain. CASPR2 and GPR37 mainly interacted with the PDZ3 and PDZ11 domains of MUPP1, respectively. Compared to GPR37, GPR37(R558Q) slightly interacted with MUPP1 and caused dendritic alteration. GPR37, but not GPR37(R558Q) nor GPR37-deltaC which lacks its PDZ binding domain, was transported to the cell surface by MUPP1. In primary hippocampal neurons, GPR37 co-localized with MUPP1 and CASPR2 at the synapse, but not GPR37(R558Q). Thus, ASD-related mutation of GPR37 may cause the impaired CASPR2-MUPP1-GPR37 complex on the dendrites associated with one of the pathogenesis of ASD. This article is protected by copyright. All rights reserved.
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9. Vahabzadeh A, Landino SM, Finger BC, Carlezon WA, Jr., McDougle CJ. {{Neural targets in the study and treatment of social cognition in autism spectrum disorder}}. {Handb Exp Pharmacol};2015;228:309-334.
The purpose of this chapter is to present results from recent research on social cognition in autism spectrum disorder (ASD). The clinical phenomenology and neuroanatomical circuitry of ASD are first briefly described. The neuropharmacology of social cognition in animal models of ASD and humans is then addressed. Next, preclinical and clinical research on the neurohormone oxytocin is reviewed. This is followed by a presentation of results from preclinical and clinical studies on the excitatory amino acid glutamate. Finally, the role of neuroinflammation in ASD is addressed from the perspectives of preclinical neuroscience and research involving humans with ASD.
