1. Braukmann R, Lloyd-Fox S, Blasi A, Johnson MH, Bekkering H, Buitelaar JK, Hunnius S. {{Diminished socially selective neural processing in 5-month-old infants at high familial risk of autism}}. {Eur J Neurosci}. 2017.
The social and communicative difficulties that characterize autism spectrum disorder (ASD) are considered the most striking feature of the disorder. Research has reported that individuals with ASD show abnormalities in the brain regions associated with the processing of social information. Importantly, a recent study using functional near-infrared spectroscopy (fNIRS) found the first evidence of atypicalities in the neural processing of social information in 4- to 6-month-old infants at high familial risk of ASD. These findings provide an important step in the search for early markers of ASD and highlight the potential for neuroimaging techniques to detect atypical patterns of neural activity prior to the manifestation of most behavioural symptoms. This study aimed to extend the findings of reduced neural sensitivity to social stimuli in an independent cohort. Twenty-nine 5-month-old infants (13 low-risk infants, 16 high-risk infants) were presented with social and non-social visual stimuli, similar to the previous experiment. Importantly, a non-social dynamic motion control condition was introduced allowing the comparison between social dynamic and non-social, static, as well as dynamic stimuli. We found that while low-risk infants showed activation to social stimuli in the right posterior temporal cortex, this activation was reduced in infants at high risk of ASD. Although the current sample size was relatively small, our results replicate and extend previous work and provide evidence for a social processing difference in infants at risk of autism. Future research will determine whether these differences relate to an eventual ASD diagnosis or may rather reflect the broader autism phenotype.
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2. Daniels J, Schwartz J, Albert N, Du M, Wall DP. {{The GapMap project: a mobile surveillance system to map diagnosed autism cases and gaps in autism services globally}}. {Mol Autism}. 2017; 8: 55.
Although the number of autism diagnoses is on the rise, we have no evidence-based tracking of size and severity of gaps in access to autism-related resources, nor do we have methods to geographically triangulate the locations of the widest gaps in either the US or elsewhere across the globe. To combat these related issues of (1) mapping diagnosed cases of autism and (2) quantifying gaps in access to key intervention services, we have constructed a crowd-based mobile platform called « GapMap » (http://gapmap.stanford.edu) for real-time tracking of autism prevalence and autism-related resources that can be accessed from any mobile device with cellular or wireless connectivity. Now in beta, our aim is for this Android/iOS compatible mobile tool to simultaneously crowd-enroll the massive and growing community of families with autism to capture geographic, diagnostic, and resource usage information while automatically computing prevalence at granular geographical scales to yield a more complete and dynamic understanding of autism resource epidemiology.
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3. Houghton K, Schuchard J, Lewis C, Thompson CK. {{Corrigendum to « Promoting child-initiated social-communication in children with autism: Son-rise program intervention effects » [J. Commun. Disord. 46/5-6 (2013) 495-506]}}. {J Commun Disord}. 2017; 70: 61.
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4. Lloyd-Fox S, Blasi A, Pasco G, Gliga T, Jones EJH, Murphy DGM, Elwell CE, Charman T, Johnson MH. {{Cortical responses before 6 months of life associate with later autism}}. {Eur J Neurosci}. 2017.
Autism spectrum disorder (ASD) is a common, highly heritable, developmental disorder and later-born siblings of diagnosed children are at higher risk of developing ASD than the general population. Although the emergence of behavioural symptoms of ASD in toddlerhood is well characterized, far less is known about development during the first months of life of infants at familial risk. In a prospective longitudinal study of infants at familial risk followed to 36 months, we measured functional near-infrared spectroscopy (fNIRS) brain responses to social videos of people (i.e. peek-a-boo) compared to non-social images (vehicles) and human vocalizations compared to non-vocal sounds. At 4-6 months, infants who went on to develop ASD at 3 years (N = 5) evidenced-reduced activation to visual social stimuli relative to low-risk infants (N = 16) across inferior frontal (IFG) and posterior temporal (pSTS-TPJ) regions of the cortex. Furthermore, these infants also showed reduced activation to vocal sounds and enhanced activation to non-vocal sounds within left lateralized temporal (aMTG-STG/pSTS-TPJ) regions compared with low-risk infants and high-risk infants who did not develop ASD (N = 15). The degree of activation to both the visual and auditory stimuli correlated with parent-reported ASD symptomology in toddlerhood. These preliminary findings are consistent with later atypical social brain responses seen in children and adults with ASD, and highlight the need for further work interrogating atypical processing in early infancy and how it may relate to later social interaction and communication difficulties characteristic of ASD.
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5. Moosa A, Shu H, Sarachana T, Hu VW. {{Are endocrine disrupting compounds environmental risk factors for autism spectrum disorder?}}. {Horm Behav}. 2017.
Recent research on the etiology of autism spectrum disorder (ASD) has shifted in part from a singular focus on genetic causes to the involvement of environmental factors and their gene interactions. This shift in focus is a result of the rapidly increasing prevalence of ASD coupled with the incomplete penetrance of this disorder in monozygotic twins. One such area of environmentally focused research is the association of exposures to endocrine disrupting compounds (EDCs) with elevated risk for ASD. EDCs are exogenous chemicals that can alter endogenous hormone activity and homeostasis, thus potentially disrupting the action of sex and other natural hormones at all stages of human development. Inasmuch as sex hormones play a fundamental role in brain development and sexual differentiation, exposure to EDCs in utero during critical stages of development can have lasting neurological and other physiological influences on the developing fetus and, ultimately, the child as well as adult. This review will focus on the possible contributions of EDCs to autism risk and pathogenesis by first discussing the influence of endogenous sex hormones on the autistic phenotype, followed by a review of documented human exposures to EDCs and associations with behaviors relevant to ASD. Mechanistic links between EDC exposures and aberrant neurodevelopment and behaviors are then considered, with emphasis on EDC-induced transcriptional profiles derived from animal and cellular studies. Finally, this review will discuss possible mechanisms through which EDC exposure can lead to persistent changes in gene expression and phenotype, which may in turn contribute to transgenerational inheritance of ASD.
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6. Mous SE, Overwater IE, Vidal Gato R, Duvekot J, Ten Hoopen LW, Lequin MH, de Wit MY, Dieleman GC. {{Cortical dysplasia and autistic trait severity in children with Tuberous Sclerosis Complex: a clinical epidemiological study}}. {Eur Child Adolesc Psychiatry}. 2017.
Tuberous Sclerosis Complex (TSC) is characterized by a high prevalence of autism spectrum disorders (ASD). Little is known about the relation between cortical dysplasia and ASD severity in TSC. We assessed ASD severity (using the Autism Diagnostic Observation Scale), tuber and radial migration line (RML) count and location, and cognitive functioning in 52 children with TSC and performed regression and mediation analyses. Tuber and RML count were strongly positively related to ASD severity. However, when correcting for cognitive functioning, the majority of associations became insignificant and only total tuber count remained associated to the severity of restricted/repetitive behaviors. Occipital RML count remained associated with overall ASD severity, and social communication/interaction deficit severity specifically. This study shows the important explanatory role of cognitive functioning in the association between cortical dysplasia and ASD severity, and the relevance of separately studying the two ASD subdomains.
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7. Olivito G, Lupo M, Laghi F, Clausi S, Baiocco R, Cercignani M, Bozzali M, Leggio M. {{Lobular patterns of cerebellar resting-state connectivity in adults with Autism Spectrum Disorder}}. {Eur J Neurosci}. 2017.
Autism spectrum disorder is a neurodevelopmental disorder characterized by core deficits in social functioning. Core autistics traits refer to poor social and imagination skills, poor attention-switching/strong focus of attention, exceptional attention to detail, as expressed by the autism-spectrum quotient. Over the years, the importance of the cerebellum in the aetiology of autism spectrum disorder has been acknowledged. Neuroimaging studies have provided a strong support to this view, showing both structural and functional connectivity alterations to affect the cerebellum in autism spectrum disorder. According to the underconnectivity theory, disrupted connectivity within cerebello-cerebral networks has been specifically implicated in the aetiology of autism spectrum disorder. However, inconsistent results have been generated across studies. In this study, an integrated approach has been used in a selected population of adults with autism spectrum disorder to analyse both cerebellar morphometry and functional connectivity. In individuals with autism spectrum disorder, a decreased cerebellar grey matter volume affected the right Crus II, a region showing extensive connections with cerebral areas related to social functions. This grey matter reduction correlates with the degree of autistic traits as measured by autism-spectrum quotient. Interestingly, altered functional connectivity was found between the reduced cerebellar Crus II and contralateral cerebral regions, such as frontal and temporal areas. Overall, the present data suggest that adults with autism spectrum disorder present with specific cerebellar structural alterations that may affect functional connectivity within cerebello-cerebral modules relevant to social processing and account for core autistics traits.
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8. Sabuncuoglu O. {{Towards a further understanding of prenatal thyroid theory of homosexuality: Autoimmune thyroiditis, polycystic ovary syndrome, autism and low birth weight}}. {Ment Illn}. 2017; 9(2): 7325.
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9. Southby K, Robinson O. {{Information, Advocacy and Signposting as a Low-Level Support for Adults with High-Functioning Autism Spectrum Disorder: An Example from the UK}}. {J Autism Dev Disord}. 2017.
‘Low-level’ support is championed to support adults with high functioning autism spectrum disorder (HFASD) to achieve good quality health and social care, yet research in the area is sparse. Drawing on semi-structured interview data, this paper considers the efficacy of an intervention to provide low-level support to adults with HFASD with little or no funded support. The intervention led to a number of perceived positive outcomes for adults with HFASD, their families, and service providers in the city, including increased access to education, volunteering, support and information, socialising, improved health and wellbeing, and managing day-to-day. Although many of life’s difficulties still persisted, the intervention helped service users overcome barriers to availing further support, possibly leading to beneficial outcomes down the line.
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10. Tryfon A, Foster NEV, Sharda M, Hyde KL. {{Speech perception in autism spectrum disorder: An activation likelihood estimation meta-analysis}}. {Behav Brain Res}. 2018; 338: 118-27.
Autism spectrum disorder (ASD) is often characterized by atypical language profiles and auditory and speech processing. These can contribute to aberrant language and social communication skills in ASD. The study of the neural basis of speech perception in ASD can serve as a potential neurobiological marker of ASD early on, but mixed results across studies renders it difficult to find a reliable neural characterization of speech processing in ASD. To this aim, the present study examined the functional neural basis of speech perception in ASD versus typical development (TD) using an activation likelihood estimation (ALE) meta-analysis of 18 qualifying studies. The present study included separate analyses for TD and ASD, which allowed us to examine patterns of within-group brain activation as well as both common and distinct patterns of brain activation across the ASD and TD groups. Overall, ASD and TD showed mostly common brain activation of speech processing in bilateral superior temporal gyrus (STG) and left inferior frontal gyrus (IFG). However, the results revealed trends for some distinct activation in the TD group showing additional activation in higher-order brain areas including left superior frontal gyrus (SFG), left medial frontal gyrus (MFG), and right IFG. These results provide a more reliable neural characterization of speech processing in ASD relative to previous single neuroimaging studies and motivate future work to investigate how these brain signatures relate to behavioral measures of speech processing in ASD.
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11. West KL, Leezenbaum NB, Northrup JB, Iverson JM. {{The Relation Between Walking and Language in Infant Siblings of Children With Autism Spectrum Disorder}}. {Child Dev}. 2017.
In typical development, walk onset is accompanied by increased language growth (e.g., Walle & Campos, 2014). The present study explored whether this relation may be disrupted in the infant siblings of children with autism spectrum disorder (ASD; heightened risk of receiving an ASD diagnosis; HR), a population exhibiting substantial variability in motor and language development (e.g., Gamliel, Yirmiya, & Sigman, 2007; Landa & Garrett-Mayer, 2006). Receptive and expressive language were examined across the transition to walking in three groups of HR infants (no diagnosis, language delay, and ASD; N = 91, 8-18 months) and in infants with no family history of ASD (N = 25; 9-15 months). Only infants with an eventual ASD diagnosis did not show increased language growth following walk onset.
