Implications For Autism Research Articles

Topic modeling for multi-omic integration in the human gut microbiome and implications for Autism

While healthy gut microbiomes are critical to human health, pertinent microbial processes remain largely undefined, partially due to differential bias among profiling techniques. By simultaneously integrating multiple profiling methods, multi-omic analysis can define generalizable microbial processes, and is especially useful in understanding complex conditions such as Autism. Challenges with integrating heterogeneous data produced by multiple profiling methods can be overcome using Latent Dirichlet Allocation (LDA), a promising natural language processing technique that identifies topics in heterogeneous documents. In this study, we apply LDA to multi-omic microbial data (16S rRNA amplicon, shotgun metagenomic, shotgun metatranscriptomic, and untargeted metabolomic profiling) from the stool of 81 children with and without Autism. We identify topics, or microbial processes, that summarize complex phenomena occurring within gut microbial communities. We then subset stool samples by topic distribution, and identify metabolites, specifically neurotransmitter precursors and fatty acid derivatives, that differ significantly between children with and without Autism. We identify clusters of topics, deemed “cross-omic topics”, which we hypothesize are representative of generalizable microbial processes observable regardless of profiling method. Interpreting topics, we find each represents a particular diet, and we heuristically label each cross-omic topic as: healthy/general function, age-associated function, transcriptional regulation, and opportunistic pathogenesis.

In Context: A Developmental Model of Reward Processing, With Implications for Autism and Sensitive Periods

Differences in reward processing have been associated with numerous psychiatric disorders, including autism and attention-deficit/hyperactivity disorder (ADHD). Many attempts to understand reward processing characterize differences in clinical populations after disorder onset; however, divergence may begin much earlier. In fact, the typical developmental progression of reward processing in infancy and early childhood is poorly understood. We re-conceptualize classic infant developmental constructs such as preferential looking into a Six-Component Developmental Model of Reward Processing: an infant- and young child-focused framework to guide research and assessment of reward processing across development. The extant developmental literature including recent textbooks, systematic reviews, and meta-analyses was reviewed to build a conceptual framework. We describe experimental paradigms to assess each developmental component of reward processing longitudinally from infancy. A timeline of each component's emergence was estimated. Six components of reward processing were identified-association, discrimination, preference/valuation, effort, anticipation, and response. Selected evidence suggests emergence between birth and 6 months. Application of this model to autism led to a reinterpretation of existing disparate results, and illuminated a path to study the developmental processes underlying a popular hypothesis of autism, the motivation hypothesis. Current evidence further suggests that a sensitive period may exist for the emergence of reward processing. The proposed framework offers a useful reconceptualization of the extant literature. Future longitudinal work using the suggested experimental paradigms with high-risk populations could elucidate the developmental trajectory of the components and timing of potential sensitive period(s) for each component.

Anti‐Epileptic Drug and Teratogen Valproic Acid Induces Microglial Cell Death in a Valproic Acid Murine Model of Autism

Autism Spectrum Disorder (ASD) is a neurodevelopmental condition that affects approximately 1 in 44 children in North America, and its association with neuronal connectivity is an area of intense research. Valproic acid (VPA) is a multi‐target drug widely used to treat epilepsy. It is classified as a teratogen and as a histone deacetylase inhibitor (HDACi) and fetal exposure to VPA increases the risk of ASD. The VPA model has been well characterized for behavioral and neuronal deficits, including hyperconnectivity. The cause of hyperconnectivity is poorly understood however, it is speculated that lack of pruning may be partly responsible for this anomaly. Microglia, the principal immune cells of CNS regulate dendrite and synapse formation during early brain development. The effect of VPA on microglia during early development has not been well characterized and may provide potential hints regarding the etiology of this disorder. Preliminary studies from our lab indicate that VPA reduces microglial number during peak periods of postnatal synaptogenesis in the mouse brain primary cortex. Nevertheless, the cause of this reduction is not known. Therefore, in this study, we determined the mechanism for reduced microglial numbers in the VPA model of autism.Pregnant BALBc mice were administered 600 mg/kg of VPA by subcutaneous injection on day 13.5 of gestation. We harvested the mice brains at embryonic (E) day 14, E17, and postnatal day 1 (PD1). Brain tissue was double immunolabeled for microglia (IBA1) and cell death marker (TUNEL). We found a gradual increase in TUNEL staining beginning E14 to PD1 compared to age‐matched controls. The mechanism for reduced microglial number may be due to cell death. Thus, our findings possibly have pathophysiological/pathogenic implications in autism and may, ultimately, lead to the discovery of new therapeutic target(s) for autism.

Acquired reinforcement: Implications for autism.

Integration of experimental analyses of behavior and neuroscience provides an interpretation of a substantial number of the diverse behavioral deficits observed within the autism spectrum. To that end, the behavioral and neural conditions under which experience changes the environmental guidance of behavior are first described, that is, the conditions under which learning occurs. These findings lead to the conclusion that acquired reinforcers-events that function as reinforcers as the result of individual experience-satisfy the same requirements and ultimately engage the same neural system as unconditioned reinforcers. Acquired reinforcers are critical to the development of complex behavior and some of the behavioral problems seen in autism may be due to these deficits. Specific consequences of these deficits are described-including effects on automatic reinforcement, joint control, and joint attention. Environmental as well as genetic factors can produce neurodevelopmental errors that impair acquired reinforcement and a possible such factor is identified. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Bilingualism, Executive Function, and the Brain: Implications for Autism.

Autism spectrum disorder (ASD) is associated with marked heterogeneity with respect to the development of executive function abilities. The bilingual advantage refers to the observation that individuals who speak two languages perform better on executive function tasks than monolinguals under some circumstances. There is not yet consensus, however, as to whether this advantage can be reliably demonstrated, nor is there consensus regarding under which conditions it emerges. Bilingual and monolingual children with ASD have comparable developmental outcomes, particularly in the areas of core ASD symptoms, cognitive function, and language. Still, despite the potential advantages that bilingualism may confer, clinicians commonly advise against providing a bilingual environment for children with ASD. The purpose of the present review is to provide an up-to-date assessment of the limited literature on bilingualism in children with ASD in order to inform evidence-based practice. Studies suggest a potential bilingual advantage in ASD in the areas of nonverbal intelligence quotient, adaptive functioning, and expressive vocabulary. A limited yet growing literature provides preliminary evidence for enhanced executive function ability in some children with ASD. Taken together, current evidence suggests that although a bilingual advantage may not be universally present in typical development, it may manifest under specific circumstances, conferring advantage for populations in which executive function is compromised. Further work is needed to develop consistent, evidence-based guidelines around language recommendations for families of children with ASD and to better understand the cognitive and brain mechanisms giving rise to the bilingual advantage in clinical developmental populations.

Regulation of Neural Circuit Development by Cadherin-11 Provides Implications for Autism.

Autism spectrum disorder (ASD) is a neurologic condition characterized by alterations in social interaction and communication, and restricted and/or repetitive behaviors. The classical Type II cadherins cadherin-8 (Cdh8, CDH8) and cadherin-11 (Cdh11, CDH11) have been implicated as autism risk gene candidates. To explore the role of cadherins in the etiology of autism, we investigated their expression patterns during mouse brain development and in autism-specific human tissue. In mice, expression of cadherin-8 and cadherin-11 was developmentally regulated and enriched in the cortex, hippocampus, and thalamus/striatum during the peak of dendrite formation and synaptogenesis. Both cadherins were expressed in synaptic compartments but only cadherin-8 associated with the excitatory synaptic marker neuroligin-1. Induced pluripotent stem cell (iPSC)-derived cortical neural precursor cells (NPCs) and cortical organoids generated from individuals with autism showed upregulated CDH8 expression levels, but downregulated CDH11. We used Cdh11 knock-out (KO) mice of both sexes to analyze the function of cadherin-11, which could help explain phenotypes observed in autism. Cdh11−/− hippocampal neurons exhibited increased dendritic complexity along with altered neuronal and synaptic activity. Similar to the expression profiles in human tissue, levels of cadherin-8 were significantly elevated in Cdh11 KO brains. Additionally, excitatory synaptic markers neuroligin-1 and postsynaptic density (PSD)-95 were both increased. Together, these results strongly suggest that cadherin-11 is involved in regulating the development of neuronal circuitry and that alterations in the expression levels of cadherin-11 may contribute to the etiology of autism.

Valproic acid alters the expression of HIF‐1α in embryonic brains in a valproic acid rodent model of autism

Although studies have investigated the role of Valproic acid (VPA) in impaired neurogenesis in rodent models of autism, the molecular mechanisms that underlie neural developmental changes during embryonic brain development in this model are poorly understood. Here, we employed a VPA rat model of autism to investigate the effects of VPA treatment on key enzymes of glucose oxidative metabolism namely lactate dehydrogenase (LDH), and genes of the adaptive responses including hypoxia induced factor 1 alpha (HIF-1α) in embryonic rat brain. Pregnant Wistar rats were administered 600 mg/kg of VPA by intraperitoneal injection on day 12.5 of gestation and embryonic (E) day 15, E17, E20 rat brains were assayed for the activity of LDH. E15, E17 and E20 male and female rat models of VPA-induced autism showed significantly increased whole brain activities of LDH compared to the corresponding values in control rats. In addition, valproic acid altered the expression of HIF-1α at the different embryonic time points. Our results suggest at least some of the mechanism underlying impaired neurogenesis in the VPA model maybe partly due to changes in activity of LDH and alteration of HIF-1α. The altered expression of HIF-1α regulates the expression of several enzymes and growth factors that may have pathophysiological/pathogenic implications in autism and may ultimately lead to the discovery of new therapeutic target(s) for autism.

Maternal immune activation targeted to a window of parvalbumin interneuron development improves spatial working memory: Implications for autism

Maternal immune activation (MIA) increases risk for neuropsychiatric disorders such as autism spectrum disorder (ASD) in offspring later in life through unknown causal mechanisms. Growing evidence implicates parvalbumin-containing GABAergic interneurons as a key target in rodent MIA models. We targeted a specific neurodevelopmental window of parvalbumin interneurons in a mouse MIA model to examine effects on spatial working memory, a key domain in ASD that can manifest as either impairments or improvements both clinically and in animal models.Pregnant dams received three consecutive intraperitoneal injections of Polyinosinic:polycytidylic acid (poly(I:C), 5 mg/kg) at gestational days 13, 14 and 15. Spatial working memory was assessed in young adult offspring using touchscreen operant chambers and the Trial-Unique Non-matching to Location (TUNL) task. Anxiety, novelty seeking and short-term memory were assessed using Elevated Plus Maze (EPM) and Y-maze novelty preference tasks. Fluorescent immunohistochemistry was used to assess hippocampal parvalbumin cell density, intensity and co-expression with perineuronal nets. qPCR was used to assess the expression of putatively implicated gene pathways.MIA targeting a window of parvalbumin interneuron development increased spatial working memory performance on the TUNL touchscreen task which was not influenced by anxiety or novelty seeking behaviour. The model reduced fetal mRNA levels of Gad1 and adult hippocampal mRNA levels of Pvalb and the distribution of low intensity parvalbumin interneurons was altered.We speculate a specific timing window for parvalbumin interneuron development underpins the apparently paradoxical improved spatial working memory phenotype found both across several rodent models of autism and clinically in ASD.

Valproic Acid Alters Activities of Key Enzymes of Glucose Oxidative Metabolism, Citric Acid Cycle and Neurotransmitter Synthesis in Embryonic Rat Brain

Although studies have investigated the role of gamma‐aminobutyric acid (GABA)ergic signaling in rodent neural development and behaviors relevant to autism, the energetics that underlie neural developmental changes are poorly understood. Here, we employed a valproic acid (VPA) rat model of autism to investigate the effects of VPA treatment on key enzymes of glucose oxidative metabolism and citric acid cycle (namely lactate dehydrogenase (LDH), malate dehydrogenase (MDH) and glutamate dehydrogenase (GDH)) in rat brain. Pregnant Wistar rats were administered 600 mg/kg of VPA by intraperitoneal injection on day 12.5 of gestation and embryonic (E) day 15 and E17 rat brains were assayed for the activities of the enzymes. Both E15 and E17 male and female rat models of VPA‐induced autism showed significantly changed whole brain activities of the enzymes studied compared to the corresponding values in control rats. The dysregulated GDH activity could alter the excitatory‐inhibitory balance in the brain of embryonic rats during development. Thus, our findings may have pathophysiological/pathogenic implications in autism and may ultimately lead to the discovery of new therapeutic target(s) for autism.Support or Funding InformationSeed Grant Idaho State University College of Pharmacy

Neuroligin-3 and neuroligin-4x promote nanoscopic growth cone actin reorganization in early neurodevelopment with implications for autism

Retrospective review.To evaluate gender-related differences in compensatory recruitment to progressive sagittal malalignment.Recent research has elucidated compensatory mechanisms recruited in response to sagittal malalignment, but gender-specific differences in compensatory recruitment patterns is unknown.Single-center study of patients with full body x-rays. A female group was propensity matched by age, body mass index (BMI), and pelvic incidence (PI) to a male group. Patients were then stratified into five groups of progressive PI–lumbar lordosis (LL) mismatch (<0°, 0°–10°, 10°–20°, 20°–30°, >30°). Differences between PI-LL groups were assessed with analysis of variance, and between genders by unpaired t test. Knee flexion to pelvic tilt (PT) ratio was computed and compared between genders. Multivariate regression to develop predictive models for PT was performed for each gender, first with spinopelvic parameters and subsequently with inclusion of lower limb parameters.A total of 942 patient visits were included: 471 females (mean age 54 years, BMI 27, PI 51°) and 471 males (mean age 52 years, BMI 27, PI 51°). At the lowest level of malalignment, females had greater PT and less knee flexion. With progressive malalignment, females continued to exhibit a pattern of greater pelvic retroversion and less knee flexion compared to males. Hip extension was higher in females with progressive PI-LL mismatch groups. Both genders progressively recruited knee flexion and pelvic retroversion with increased PI-LL mismatch, except that at the higher PI-LL mismatch groups, only males continued to recruit knee flexion (all p < .05). Inclusion of lower limbs in the regression for PT markedly improved correlation coefficients for females but not for males.With progressive sagittal malalignment, men recruit more knee flexion and women recruit more pelvic tilt and hip extension. Knee flexion is a possible mechanism to gain pelvic tilt for females whereas for males, knee flexion is an independent compensatory mechanism.

Syllogistic reasoning reveals reduced bias in people with higher autistic-like traits from the general population.

Recent theories of autism have emphasised the cognitive strengths and weaknesses in those with autism, which are also seen to some degree in non-clinical samples with higher autistic-like traits. The dual process theory of autism proposes that people with autism and non-clinical people with a higher degree of autistic-like traits have a propensity to show reduced intuitive processing (automatic and typically faster) alongside enhanced propensity towards deliberative processing (dependent on general cognitive ability and typically slower). This study aimed to further test the dual process theory of autism by investigating syllogistic reasoning (whether a conclusion can be logically deduced from two propositions) in addition to the cognitive reflection test (correct responses to which reflect deliberative processing over-riding intuitive processing) with respect to the degree of autistic-like traits and general cognitive ability in a non-clinical sample of 189 adults. Results showed that higher levels of autistic-like traits were related to lower levels of intuitive processing and higher levels of deliberative processing, which was found across both the syllogistic reasoning and cognitive reflection test measures - over and above the effect of general cognitive ability. The findings are consistent with the dual process theory of autism, and implications for autism are discussed.

Maternal Exposure to Childhood Abuse is Associated with Mate Selection: Implications for Autism in Offspring.

Maternal experience of childhood abuse has been associated with offspring autism. To explore whether familial tendency towards autistic traits-presumably related to genetic predisposition-accounts for this association, we examined whether women who experienced childhood abuse were more likely to select mates with high levels of autistic traits, and whether parental autistic traits accounted for the association of maternal abuse and offspring autism in 209 autism cases and 833 controls. Maternal childhood abuse was strongly associated with high paternal autistic traits (severe abuse, OR=3.98, 95% CI=1.26, 8.31). Maternal and paternal autistic traits accounted for 21% of the association between maternal abuse and offspring autism. These results provide evidence that childhood abuse affects mate selection, with implications for offspring health.

Role of the cerebellum in high stages of motor planning hierarchy.

Motor planning is not a monolithic process, and distinct stages of motor planning are responsible for encoding different levels of abstractness. However, how these distinct components are mapped into different neural substrates remains an open question. We studied one of these high-level motor planning components, defined as second-order motor planning, in a patient (R.G.) with an extremely rare case of cerebellar agenesis but without any other cortical malformations. Second-order motor planning dictates that when two acts must be performed sequentially, planning of the second act can influence execution of the first. We used an optoelectronic system for kinematic analysis to compare R.G.'s performance with age-matched controls in a second-order motor planning task. The first act was to reach for an object, and the second was to place it into a small or large container. Our results showed that despite the expected difficulties in fine-motor skills, second-order motor planning (i.e., the ability to modulate the first act as a function of the nature of the second act) was preserved even in the patient with congenital absence of the cerebellum. These results open new intriguing speculations about the role of the cerebellum in motor planning abilities. Although prudence is imperative when suggesting conclusions made on the basis of single-case findings, this evidence suggests fascinating hypotheses about the neural circuits that support distinct stages of the motor planning hierarchy, and regarding the functional role of second-order motor planning in motor cognition and its potential dysfunction in autism.NEW & NOTEWORTHY Traditionally, the cerebellum was considered essential for motor planning. By studying an extremely rare patient with cerebellar agenesis and a group of neurotypical controls, we found that high stages of the motor planning hierarchy can be preserved even in this patient with congenital absence of the cerebellum. Our results provide interesting insights that shed light on the neural circuits supporting distinct levels of motor planning. Furthermore, the results are intriguing because of their potential clinical implications in autism.

Prevention of behavioral deficits in rats exposed to folate receptor antibodies: implication in autism.

Folate receptor alpha (FRα) autoantibodies have been associated with fetal abnormalities and cerebral folate deficiency-related developmental disorders. Over 70% of the children with autism spectrum disorders (ASD) are positive for these autoantibodies and high-dose folinic acid is beneficial in treating these children. Here we show that antibodies (Abs) to the rat FRα administered during gestation produce communication, learning and cognitive deficits in a rat model that can be prevented by folinic acid and dexamethasone. FRα Ab can trigger inflammation as well as block folate transport to the fetus and to the developing brain to produce the functional deficits. In humans, exposure to FRα autoantibodies during fetal development and infancy could contribute to brain dysfunction such as that seen in ASD and other developmental disorders. Identifying women positive for the autoantibody and treating them with high-dose folinic acid along with other interventions to lower the autoantibody titer are effective strategies that may be considered to reduce the risk of having a child with developmental deficits.

A Neuroeconomic Theory of Attention- and Task-Switching with Implications for Autism and ADHD

This paper presents a theoretical and neurobiologically-grounded model of attention- and task-switching in response to novel stimuli. Within this framework, I show how key features of autism and of attention-deficit/hyperactivity disorder (ADHD) can be explained by simple “biases” (which can be alternatively interpreted as preference shifters) with regards to how agents value potential diversions in relation to a preoccurring task. Specifically, the theory suggests that diversions of this sort are systematically undervalued in autism and overvalued in ADHD, giving rise to the atypically low attention- and task-switching propensities observed in autism and the reverse in ADHD. While making a broader case for the potential value of economic theory as a lens through which to understand such psychiatric conditions, I draw on a range of formal economic concepts — opportunity cost, willingness-to-pay, risk aversion, time preferences, payoff/cost elasticities — to capture many other documented patterns in autism and in ADHD. In doing so, the model motivates a new classification of autism and ADHD as opposites in that their behavioral symptoms arise from opposite underlying biases. That said, the results also show how many of their symptoms — including some in the domain of social behavior — can overlap, if crudely defined, suggesting a potential clinical benefit from more precise diagnostic criteria.

REMOVED: Evidence for a decrease in dendrites of pyramidal cells in neonatal thalamic lesioned rat's prefrontal cortex: Implication in Autism and Schizophrenia

This article has been removed: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our‐business/policies/article‐withdrawal)This meeting abstract has been removed by the Publisher. Due to an administrative error, abstracts that were not presented at the ISDN 2014 meeting were inadvertently published in the meeting's abstract supplement. The Publisher apologizes to the authors and readers for this error.

Atypical emotional anticipation in high-functioning autism.

BackgroundUnderstanding and anticipating others’ mental or emotional states relies on the processing of social cues, such as dynamic facial expressions. Individuals with high-functioning autism (HFA) may process these cues differently from individuals with typical development (TD) and purportedly use a ‘mechanistic’ rather than a ‘mentalistic’ approach, involving rule- and contingency-based interpretations of the stimuli. The study primarily aimed at examining whether the judgments of facial expressions made by individuals with TD and HFA would be similarly affected by the immediately preceding dynamic perceptual history of that face. A second aim was to explore possible differences in the mechanisms underpinning the perceptual judgments in the two groups.MethodsTwenty-two adults with HFA and with TD, matched for age, gender and IQ, were tested in three experiments in which dynamic, ‘ecologically valid’ offsets of happy and angry facial expressions were presented. Participants evaluated the expression depicted in the last frame of the video clip by using a 5-point scale ranging from slightly angry via neutral to slightly happy. Specific experimental manipulations prior to the final facial expression of the video clip allowed examining contributions of bottom-up mechanisms (sequential contrast/context effects and representational momentum) and a top-down mechanism (emotional anticipation) to distortions in the perception of the final expression.ResultsIn experiment 1, the two groups showed a very similar perceptual bias for the final expression of joy-to-neutral and anger-to-neutral videos (overshoot bias). In experiment 2, a change in the actor’s identity during the clip removed the bias in the TD group, but not in the HFA group. In experiment 3, neutral-to-joy/anger-to-neutral sequences generated an undershoot bias (opposite to the overshoot) in the TD group, whereas no bias was observed in the HFA group.ConclusionsWe argue that in TD individuals the perceptual judgments of other’s facial expressions were underpinned by an automatic emotional anticipation mechanism. In contrast, HFA individuals were primarily influenced by visual features, most notably the contrast between the start and end expressions, or pattern extrapolation. We critically discuss the proposition that automatic emotional anticipation may be induced by motor simulation of the perceived dynamic facial expressions and discuss its implications for autism.

Can Music Increase Empathy? Interpreting Musical Experience Through the Empathizing–Systemizing (E-S) Theory: Implications for Autism

Recent research has provided evidence that musical interaction can promote empathy. Yet little is known about the underlying intrapersonal and social psychological processes that are involved when this occurs. For example, which types of music increase empathy and which types decrease it; what role, if any, does empathy play in determining individual differences in musical preference, perception, and performance; or, how do these psychological underpinnings help explain the musical experiences of people with autism spectrum conditions (ASC). To address these questions we employ the Empathizing–Systemizing (E-S) theory as a fruitful framework in which to understand these music-related phenomena. Specifically, we explore how individual differences in musical preference, perception, and performance can be explained by E-S theory. We provide examples from open-ended descriptions of strong musical experiences to demonstrate the ways in which empathy and music inter-relate. Importantly, we discuss the implications for the study of autism, and for how music therapists and clinicians can use music as a tool in their work with individuals diagnosed with ASC.

Monogenic mouse models of social dysfunction: Implications for autism

Autism is a pervasive disorder characterized by a complex symptomatology, based principally on social dysfunction. The disorder has a highly complex, largely genetic etiology, involving an impressive variety of genes, the precise contributions of which still remain to be determined. For this reason, a reductionist approach to the study of autism has been proposed, employing monogenic animal models of social dysfunction, either by targeting a candidate gene, or by mimicking a single-gene disorder characterized by autistic symptoms. In the present review, we discuss this monogenic approach by comparing examples of each strategy: the mu opioid receptor knock-out (KO) mouse line, which targets the opioid system (known to be involved in the control of social behaviors); and the Fmr1-KO mouse, a model for Fragile X syndrome (a neurodevelopmental syndrome that includes autistic symptoms). The autistic-relevant behavioral phenotypes of the mu-opioid and Fmr1-KO mouse lines are described here, summarizing previous work by our research group and others, but also providing novel experimental evidence. Relevant factors influencing the validity of the two models, such as sex differences and age at testing, are also addressed, permitting an extensive evaluation of the advantages and limits of monogenic mouse models for autism.

Autism, social cognition and superior temporal sulcus

Results on brain imaging studies have led to a better understanding of the neural circuits involved in social cognition and its implication in autism spectrum disorders(ASD). It has been shown that the superior temporal sulcus(STS)is highly implicated in social processes, from perception of socially relevant information, such as body movements or eye gaze, to more complex social cognition processes. Furthermore, several multimodal brain imaging results point to anatomo-functional abnormalities in the STS in both children and adults with ASD. These results are highly consistent with social impairments in ASD, among which eye gaze perception is particularly relevant. Gaze abnormalities can now be objectively measured using eye-tracking methodology, leading to a better characterization of social perception impairments in autism. Moreover, these gaze abnormalities have been associated with STS abnormalities in ASD. Based on these results, our hypothesis is that anatomo-functional anomalies in the STS occurring early across brain development could constitute the first step in the cascade of neural dysfunction underlying autism. In the present work, we’ll review recent data of STS contribution to normal social cognition and it’s implication in autism.