Social Skills Teaching for Individuals with Autism Spectrum Disorder: a Systematic Review

Radley, Keith C.; Dart, Evan H.; Brennan, Kayleigh J.; Helbig, Kate A.; Lehman, Erica; Silberman, Magenta; Mendanhall, Kai

doi:10.1007/s41252-020-00170-x

Cited by 25 publications

(6 citation statements)

References 66 publications

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“…These trends were concordant with previous observations in different ASD-like models, including MIA and VPA offspring, where males tend to manifest more pronounced deficits in social interaction abilities (82, 83). In the context of the three-chamber test, these results are indicators of impaired social skills, which are widely recognized to correlate with recurring ASDlike behaviors in both humans and mice (84)(85)(86).…”

Section: Discussionmentioning

confidence: 99%

Gestational hypothyroxinemia induces ASD-like phenotypes in behavior, proinflammatory markers, and glutamatergic protein expression in mouse offspring of both sexes

González-Madrid,

Rangel-Ramírez,

Opazo

et al. 2024

Front. Endocrinol.

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BackgroundThe prevalence of autism spectrum disorder (ASD) has significantly risen in the past three decades, prompting researchers to explore the potential contributions of environmental factors during pregnancy to ASD development. One such factor of interest is gestational hypothyroxinemia (HTX), a frequent condition in pregnancy associated with cognitive impairments in the offspring. While retrospective human studies have linked gestational HTX to autistic traits, the cellular and molecular mechanisms underlying the development of ASD-like phenotypes remain poorly understood. This study used a mouse model of gestational HTX to evaluate ASD-like phenotypes in the offspring.MethodsTo induce gestational HTX, pregnant mice were treated with 2-mercapto-1-methylimidazole (MMI), a thyroid hormones synthesis inhibitor, in the tap-drinking water from embryonic days (E) 10 to E14. A separate group received MMI along with a daily subcutaneous injection of T4, while the control group received regular tap water during the entire pregnancy. Female and male offspring underwent assessments for repetitive, anxious, and social behaviors from postnatal day (P) 55 to P64. On P65, mice were euthanized for the evaluation of ASD-related inflammatory markers in blood, spleen, and specific brain regions. Additionally, the expression of glutamatergic proteins (NLGN3 and HOMER1) was analyzed in the prefrontal cortex and hippocampus.ResultsThe HTX-offspring exhibited anxious-like behavior, a subordinate state, and impaired social interactions. Subsequently, both female and male HTX-offspring displayed elevated proinflammatory cytokines in blood, including IL-1β, IL-6, IL-17A, and TNF-α, while only males showed reduced levels of IL-10. The spleen of HTX-offspring of both sexes showed increased Th17/Treg ratio and M1-like macrophages. In the prefrontal cortex and hippocampus of male HTX-offspring, elevated levels of IL-17A and reduced IL-10 were observed, accompanied by increased expression of hippocampal NLGN3 and HOMER1. All these observations were compared to those observed in the Control-offspring. Notably, the supplementation with T4 during the MMI treatment prevents the development of the observed phenotypes. Correlation analysis revealed an association between maternal T4 levels and specific ASD-like outcomes.DiscussionThis study validates human observations, demonstrating for the first time that gestational HTX induces ASD-like phenotypes in the offspring, highlighting the need of monitoring thyroid function during pregnancy.

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Section: Discussionmentioning

confidence: 99%

Gestational hypothyroxinemia induces ASD-like phenotypes in behavior, proinflammatory markers, and glutamatergic protein expression in mouse offspring of both sexes

González-Madrid,

Rangel-Ramírez,

Opazo

et al. 2024

Front. Endocrinol.

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“…In the context of the three-chamber setup, we interpret these results as indicators of impaired social skills, which hold pivotal importance for the evolutionary success of both rodents and humans. Moreover, these deficiencies in social skills are widely recognized to correlate with recurring ASDlike behaviors in both humans and mice [84][85][86].…”

Section: Discussionmentioning

confidence: 99%

Gestational hypothyroxinemia causes autistic-like behaviors, increases proinflammatory traits, and alters glutamatergic protein expression in mouse adult offspring of both sexes.

González-Madrid,

Rangel-Ramírez,

Opazo

et al. 2023

Preprint

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Prevalence of autism spectrum disorder (ASD) has increased over the past three decades. In this regard, there is growing evidence suggesting that environmental factors during pregnancy may contribute as risk factors for ASD, potentially playing a role in this rising trend. Gestational hypothyroxinemia (HTX) is an asymptomatic and frequent thyroid condition characterized by low levels of thyroxine (T4) in blood, with normal range of T3 and TSH. When this condition occurs in early pregnancy it impairs fetal neurodevelopment and diminishes cognitive capacities in the offspring. Additionally, retrospective human studies have shown that gestational HTX is associated with autistic outcomes in the offspring, however, there is an absence of knowledge about the cellular and molecular autism-like traits in the offspring gestated under gestational HTX (HTX-offspring). In this work, autistic-like phenotypes were evaluated in HTX-offspring, using a mouse model of gestational HTX. Consistent with autism-like behaviors of mice models, HTX-offspring exhibited anxiety-related behavior and impaired social interaction skills. Similar to humans, these features were more pronounced in male HTXoffspring. At the molecular level, the expression of NLGN3 and HOMER1 was increased in the prefrontal cortex and hippocampus of male HTX-offspring, compared to the offspring gestated under euthyroidism. Moreover, HTX-offspring showed increased proinflammatory cytokines in serum and an increased ratio of Th17 lymphocytes relative to T regulatory lymphocytes (Th17/Treg), as well as high neuroinflammatory-like traits in the prefrontal cortex and hippocampus, which were also more pronounced in male HTX-offspring. Notably, by administering T4 to pregnant mice during the induction of HTX, the offspring was protected from developing the observed autism-like traits. These findings support that gestational HTX constitutes a significant risk factor for the development of autism-like phenotypes in the offspring and strongly emphasizes the importance of monitoring thyroid function in early pregnancy.

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“…Explicit teaching of conversation skills – in combination with the opportunity to practise – is the backbone of Speech and Language Therapy methods for improving conversation ability – and pragmatic language more generally – in children and adults with communication difficulties (Adams et al, 2012; Timler, 2018; Winner, 2007). Conversation skills are also explicitly taught during lessons focussing on ‘Social Emotional Skills’ (DuPaul & Eckert, 1994) and as part of many ‘social skills’ curricula (Hall et al, 2018; Radley et al, 2020), which are often aimed at children with behavioural or emotional difficulties. Below, we review evidence, first, that explicit conversation skills training improves conversational ability in children who arrive at the training with clinical difficulties in conversation.…”

Section: How Do Children Become Better At Conversation?mentioning

confidence: 99%

Topic maintenance in social conversation: What children need to learn and evidence this can be taught

et al. 2023

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Individual differences in children’s social communication have been shown to mediate the relationship between poor vocabulary or grammar and behavioural difficulties. Moreover, there is increasing evidence that social communication skills predict difficulties with peers over and above vocabulary and grammar scores. The essential social communicative skills needed to maintain positive peer relationships revolve around conversation. Children with weaker conversation skills are less likely to make and maintain friendships. While helping all children to participate actively in collaborative conversations is part of school curricula, evidence-based training on how to achieve this is rarely provided for teachers. In this review, we first provide an overview of the key components of conversation skills and the cognitive abilities required to maintain them. We then present a narrative review of randomised controlled trials and experimental studies that either trained child conversation skills or included conversation skills in both training and outcome measures. Most of the studies focussed on training conversational ability in autistic children. The general finding was that verbally fluent autistic children improve following conversation training on blind-assessed reciprocal conversational ability. Only two studies were found that trained conversation skills in typically developing children with adequate controls and outcome measures, which directly assessed conversational proficiency. Both studies focussed on typically developing children who, at baseline, were in the weaker third of the mainstream classroom. Importantly, training not only improved the conversational ability of these children, it also improved their rates of lunchtime interaction with peers and their peer popularity ratings. We argue that there is considerable potential for supporting conversation skills in the classroom as a universal or Tier 1 intervention. Future research should explore whether conversation skills training would benefit the whole classroom.

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Social Skills Teaching for Individuals with Autism Spectrum Disorder: a Systematic Review

Cited by 25 publications

References 66 publications

Gestational hypothyroxinemia induces ASD-like phenotypes in behavior, proinflammatory markers, and glutamatergic protein expression in mouse offspring of both sexes

Gestational hypothyroxinemia induces ASD-like phenotypes in behavior, proinflammatory markers, and glutamatergic protein expression in mouse offspring of both sexes

Gestational hypothyroxinemia causes autistic-like behaviors, increases proinflammatory traits, and alters glutamatergic protein expression in mouse adult offspring of both sexes.

Topic maintenance in social conversation: What children need to learn and evidence this can be taught

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