1. Bennett KD, Ramasamy R, Honsberger T. {{The Effects of Covert Audio Coaching on Teaching Clerical Skills to Adolescents with Autism Spectrum Disorder}}. {J Autism Dev Disord};2012 (Jul 14)
Employment instruction for secondary students with autism spectrum disorder (ASD) has received very little attention in the professional literature. However, adults with ASD usually have difficulty maintaining employment for a variety of reasons, including problems with performing work tasks. This study used a multiple baseline design across participants to examine the effects of performance feedback on the participants’ ability to independently make photocopies. Feedback was delivered privately through a two-way radio and earbud speaker. The results support the conclusion that the intervention, covert audio coaching, was effective in increasing the participants’ accuracy in making photocopies. Specifically, participants demonstrated mastery of the skill within 4-5 sessions, and their improvements maintained for several weeks following intervention.
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2. Bowler D. {{Autism spectrum disorders (ASD)}}. {Autism};2012 (May);16(3):223-225.
3. Duerden EG, Szatmari P, Roberts SW. {{Toward a Better Understanding of Self Injurious Behaviors in Children and Adolescents with Autism Spectrum Disorders}}. {J Autism Dev Disord};2012 (Jul 14)
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4. Feczko E, Miezin FM, Constantino JN, Schlaggar BL, Petersen SE, Pruett JR, Jr. {{The hemodynamic response in children with Simplex Autism}}. {Dev Cogn Neurosci};2012 (Jun 28)
BACKGROUND: Numerous functional magnetic resonance imaging (fMRI) studies of the brain-bases of autism have demonstrated altered cortical responses in subjects with autism, relative to typical subjects, during a variety of tasks. These differences may reflect altered neuronal responses or altered hemodynamic response. This study searches for evidence of hemodynamic response differences by using a simple visual stimulus and elementary motor actions, which should elicit similar neuronal responses in patients and controls. METHODS: We acquired fMRI data from two groups of 16 children, a typical group and a group with Simplex Autism, during a simple visuomotor paradigm previously used to assess this question in other cross-group comparisons. A general linear model estimated the blood-oxygen-level-dependent (BOLD) signal time course, and repeated-measures analysis of variance tested for potential cross-group differences in the BOLD signal. RESULTS: The hemodynamic response in Simplex Autism is similar to that found in typical children. Although the sample size was small for a secondary analysis, medication appeared to have no effect on the hemodynamic response within the Simplex Autism group. CONCLUSIONS: When fMRI studies show BOLD response differences between autistic and typical subjects, these results likely reflect between-group differences in neural activity and not an altered hemodynamic response.
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5. Galvan AM, Galvez R. {{Neocortical Vasculature Abnormalities in the Fragile X Mental Retardation Syndrome}}. {Brain Res};2012 (Jul 10)
The Fragile X Syndrome (FXS) is the leading form of inherited mental retardation. To date, the most prominent neuronal phenotype associated with the syndrome is an abundance of long thin spines exhibiting an immature morphology. However, in addition to synaptic abnormalities, recent case studies have demonstrated that Fragile X (FX) patients also exhibit abnormal cerebral blood flow (CBF). To examine the role of the Fragile X Mental Retardation Protein (FMRP) in altering CBF, we examined blood vessel density (BVD) in the visual cortex of Adult and Middle-aged FX mice. Analysis of Middle-aged FX mice demonstrated elevated BVD compared to wildtype controls, suggesting that FX mice exhibit a lack of age-induced BVD plasticity. However, Adult FX and wildtype mice did not exhibit consistent differences in BVD. These data demonstrate that FMRP is required for age-induced neocortical vasculature plasticity. Furthermore, these data suggest a new role for FMRP in blood vessel regulation that would have profound implications towards appropriately timed delivery of neuronal nutrients, thus contributing to or exacerbating FX cognitive and neuronal abnormalities.
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6. Hartley SL, Seltzer MM, Hong J, Greenberg JS, Smith L, Almeida D, Coe C, Abbeduto L. {{Cortisol response to behavior problems in FMR1 premutation mothers of adolescents and adults with fragile X syndrome: A diathesis-stress model}}. {Int J Behav Dev};2012 (Jan);36(1):53-61.
Mothers of adolescents and adults with fragile X syndrome (FXS) are faced with high levels of parenting stress. The extent to which mothers are negatively impacted by this stress, however, may be influenced by their own genetic status. The present study uses a diathesis-stress model to examine the ways in which a genetic vulnerability in mothers with the premutation of the FMR1 gene interacts with child-related environmental stress to predict their morning cortisol levels. Seventy-six mothers of an adolescent or adult with FXS participated in an 8-day telephone diary study in which they reported on the behavior problems of their son or daughter with FXS each day. We analyzed salivary cortisol collected from mothers at awakening and 30 minutes after awakening on 4 of these days. The results indicated that mothers with greater genetic vulnerability had a lower level of cortisol on mornings following days when their son or daughter with FXS manifested more episodes of behavior problems, whereas mothers with less genetic risk evinced the opposite pattern of higher morning cortisol in response to their child’s behavior problems. This finding contributes to our understanding of gene-by-environment interactions and highlights the importance of interventions to alleviate parenting stress in mothers raising children with FXS.
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7. Heck DH, Lu L. {{The social life of neurons: synaptic communication deficits as a common denominator of autism, schizophrenia, and other cognitive disorders}}. {Biol Psychiatry};2012 (Aug 1);72(3):173-174.
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8. Schluter EW, Hunsaker MR, Greco CM, Willemsen R, Berman RF. {{Distribution and Frequency of Intranuclear Inclusions in Female CGG KI Mice Modeling the Fragile X Premutation}}. {Brain Res};2012 (Jul 10)
The fragile X-associated tremor/ataxia syndrome (FXTAS) is an adult-onset neurodegenerative disorder caused by CGG trinucleotide repeat expansions in the fragile X mental retardation 1 (FMR1) gene. The neuropathological hallmark of FXTAS is the presence of ubiquitin-positive intranuclear inclusions in neurons and in astroglia. Intranuclear inclusions have also been reported in the neurons of male CGG KI mice carrying an expanded CGG trinucleotide repeat and used to model FXTAS, but no study has been carried out quantifying inclusions in female CGG KI mice heterozygous for the fragile X premutation. We used histologic and immunocytochemical methods to determine the pathological features of intranuclear inclusions in astroglia and neurons. In female CGG KI mice, ubiquitin-positive intranuclear inclusions were found in neurons and astroglia throughout the brain in cortical and subcortical regions. These inclusions increased in number and became larger with advanced age and increasing CGG repeat length, supporting hypotheses that these pathologic features are progressive across the lifespan. The number of inclusions in neurons were reduced by approximately 25% in female CGG KI mice compared to male CGG KI mice, but not so low as the 50% predicted. These data emphasize the need to evaluate the neurocognitive and pathological features in female carriers of the fragile X premutation with and without FXTAS symptomatology is warranted, as this population shows similar neuropathological features present in male FXTAS patients.
