Deficits In Autism Research Articles

Neuronal subset-specific Pten-deficient mice do not exhibit deficits in sensorimotor gating processes

Background: Deficits in sensorimotor gating have been reported in individuals with autism spectrum disorder (ASD), as well as in ASD murine models. However, this behavior has been rarely examined in the neuronal subset-specific (NS)-Pten knockout (KO) model of ASD. NS-Pten KO mice exhibit hyperactivity of the PI3K/AKT/mTOR signaling pathway which is implicated in the onset of autistic deficits. This study investigates the potential relationship between PI3K/AKT/mTOR signaling and deficits in sensorimotor gating. Methods: To assess sensorimotor gating in NS-Pten KO mice we utilized a three-day paradigm. On day 1 (habituation) the mice were administered 80 repetitions of a 120-dB startle stimulus. On day 2, prepulse inhibition was measured with 90 trials of the startle stimulus that was paired with a smaller (70, 75, or 80 dB) prepulse stimulus. Day 3 was assessed one week later, consisting of randomized startle trials and trials with no stimulus and was used to determine the startle threshold. Results: No significant difference between NS-Pten KO or wildtype (WT) mice was found for habituation (p > 0.05). No significant differences were found between groups when assessing the percentage of prepulse inhibition at 70, 75, and 80 dB (p > 0.05). There was also no difference in startle threshold between groups (p > 0.05). Conclusion: Our study found that the NS-Pten KO model does not display significant deficits in sensorimotor gating processes. The present findings help to elucidate the relationship between PI3K/AKT/mTOR hyperactivation and sensory reactivity.

Gut microbiota rugulates autistic deficits in VPA induced prenatal model of autism

To amend the autistic behavior in prenatally exposed valproic acid (VPA) bytreatment with probiotic supplementation.Methods: autism induced by administration of VPA 300mg/kg, i.p. on gestation 12.5and 13 days. The offspring were weaned on postnatal (PND) day 23; separate them intosix groups, each group with six rats. I) Control group II) Autistic group III) B. Infantis (5billion cfu/gm p.o); IV) B. longum (5 billion cfu/gm, p.o); V) L. Plantarum (5 billioncfu/gm, p.o) VI) L. Bulgaricus (5 billion cfu/gm, p.o) treat the animals with probiotics onPND 23 – PND 50. Behavioral studies are performed on various postnatal days untilPND 50.Results: supplementation with probiotics PND 23 - 50 showed that there is a significantrecovery in behavioral activity in comparison to Autistic group.Conclusion: Results of our study revealed that Probiotics can influence the braindevelopment and behavior. It might be through communication between gut and brain.

The importance of social neurosciences for psychiatry

The social brain is dysfunctional in numerous stress-related psychiatric disorders. The definition of social brain networks and their susceptibility for social environmental stress. It is also reviewed how social brain networks are disrupted in schizophrenia, autism and conduct disorder. Literature search in PubMed. The social brain consists of several subnetworks that act in concert to foster empathy. Interestingly, except for the mirror neuron system, the neural networks of the social brain have been reported to be vulnerable to social environmental stress and have also been highlighted as being compromised in psychiatric disorders. As an example, schizophrenia is related to dysfunction in social perception, mentalizing, and affiliation, whereas the most pronounced deficits in autism are seen during social perception and mentalizing. Patients with conduct disorder are more prone to dysfunction in perception, affiliation and aversion. Social stress affects subnetworks also compromised in psychiatric disorders. Therefore, it is plausible that the social brain might mediate the association between social stress and psychiatric disorders. To advance ecological validity in social neuroscience, recent research has highlighted the role of hyperscanning and virtual reality as means by which amore naturalistic assessment of social interactions might be feasible.

Atypical Response Properties of the Auditory Cortex of Awake MECP2-Overexpressing Mice.

Methyl-CpG binding protein 2 (MECP2) is a gene associated with DNA methylation and has been found to be important for maintaining brain function. In humans, overexpression of MECP2 can cause a severe developmental disorder known as MECP2 duplication syndrome. However, it is still unclear whether MECP2 overexpression also causes auditory abnormalities, which are common in people with autism. MECP2-TG is a mouse model of MECP2 duplication syndrome and has been widely used for research on social difficulty and other autism-like disorders. In this study, we used a combination of multiple electrophysiological techniques to document the response properties of the auditory cortex of awake MECP2-TG mice. Our results showed that while the auditory brainstem responses are similar, cortical activity patterns including local field potentials (LFPs), multiunit activity (MUA), and single-neuron responses differ between MECP2-TG and wild-type (WT) mice. At the single-neuron level, the spike waveform of fast-spiking (FS) neurons from MECP2-TG mice is different from that of WT mice, as reflected by reduced peak/trough ratios in the transgenic mice. Both regular-spiking (RS) and FS neurons exhibited atypical response properties in MECP2-TG mice compared with WT mice, such as prolonged latency and an elevated intensity threshold; furthermore, regarding the response strength to different stimuli, MECP2-TG mice exhibited stronger responses to noise than to pure tone, while this pattern was not observed in WT mice. Our findings suggest that MECP2 overexpression can cause the auditory cortex to have atypical response properties, an implication that could be helpful for further understanding the nature of auditory deficits in autism.

Do importance instructions improve time-based prospective remembering in autism spectrum conditions?

This study explored the impact of motivation on the memory for delayed intentions (so-called, prospective memory, PM) in autistic individuals. Specifically, we were interested in the effects of personal (i.e., receiving a reward) as compared to social motivation (i.e., performing a favour for someone). Given the well-established theory of mind deficits in autism, we expected autistic individuals to benefit more strongly from personal than social importance manipulations, whereas the opposite pattern was predicted for controls. Sixty-one adolescents with autism and 61 typically developing adolescents participated, with each group distributed equally to one of the three motivation conditions of standard, social and personal reward. Participants worked on a 2-back picture-based ongoing task in which a time-based PM task was embedded. A mixed 2 (Group) x 3 (Motivation condition) analysis of covariance with age, verbal and non-verbal abilities as covariates and correct PM responses as dependent variable indicated solely a main effect of group, with controls outperforming the autism group. In contrast to our expectations, there was no main effect of condition, no significant interaction, and none of the covariates had any significant impact. However, further planned analyses revealed that controls only outperformed autistic individuals in the personal reward condition. Controls performed significantly best when a personal reward was promised, whereas there were no significant differences between the motivation conditions for autistic individuals. Findings are discussed in terms of underlying processes.

The relationship between pantomime execution and recognition across typically developing and autistic children

BackgroundMotor deficits in autism have a double aspect: on one side, they are neglected by standard diagnostic procedures, on the other they are very frequent (70%) and promising as early indicator of the syndrome. Their characterization is extremely relevant, as they could impact on social abilities based on the understanding of others’ actions. MethodFifty-two typically developing children (TD) and 13 children with autism spectrum disorder (ASD) took part to the study. Children were evaluated in pantomime execution, and in two tasks based on pantomime observation: recognition of pantomime meaning, and error recognition, with observed pantomimes that could contain spatial, temporal or body-part-as-tool errors. ResultsTD children performance in tasks based on observation appeared strongly associated to individual motor skills. In general, ASD children exhibited a poorer performance than TD in all tasks. Most interestingly, in both pantomime execution and error recognition they showed a parallel and selective prevalence of spatial errors, whose scores resulted to be correlated with the autistic symptoms severity. ConclusionsIn TD children, the capacity to decode the actions done by others relies on the observer motor repertoire. In children with autism, the parallelism between deficits in pantomime execution and recognition suggests that during action observation the motor resonance is impoverished due to an impaired motor repertoire, thus impeding a proper social contact with others.

Lepidium Sativum Seeds as a Suggested Complex Nutritional Supplement to Treat Biomarkers Related Deficits in Autism

Autism as a neurodevelopmental disorder is characterized by persistent autistic features such as impaired social communication, restricted and repetitive behavior, and intellectual disabilities. As a disorder, autism has several ubiquitous co-morbidities, among which is sleep disorders, epilepsy, attention deficit, and hyperactivity. No effective treatment for the core symptoms of autism is available until now.

Developmental trajectories of autonomic functioning in autism from birth to early childhood

Deficits in social engagement emerge in autism during the infant and toddler period and may be related to emotion regulation and stress response systems. This study examined patterns of growth in autonomic functioning related to autism diagnosis and addresses the hypothesis that there are differences in autonomic functioning related to autism in infancy. Heart rate (HR) and respiratory sinus arrhythmia (RSA) were measured at 8 time points from 1 to 72 months of age in infants later diagnosed with autism (n = 12) and a non-autistic comparison group (n = 106). Multilevel models were used to describe the developmental course of HR and RSA and to test the effect of autism diagnosis on growth trajectories. Both groups showed an expected age-related decrease in HR and increase in RSA. Groups did not differ in the rate of decrease of HR over time. However, infants with autism demonstrated a smaller linear increase in RSA, indicating slower growth in RSA over time in comparison to controls. These results suggest that differences in physiological regulation may develop with age in autism. The slowed RSA growth in autism was most evident after 18 months of age, at a time when behavioral symptoms become prominent. This is consistent with the view that RSA is a marker of functional status in autism rather than a cause of social deficits in autism.

Perfil psicomotor de crianças com transtorno do espectro autista

As alterações no funcionamento cerebral que ocorrem no Transtorno do Espectro Autista são causadas por uma desordem no desenvolvimento neurológico, podendo acarretar atrasos ou déficits de comunicação, atraso na aquisição de habilidades motoras e também nas relações sociais. Associada às alterações corticais, a redução de experiências motoras prejudica a aquisição e a qualidade dos movimentos executados por crianças com Transtorno do Espectro Autista, podendo interferir em sua autonomia. O objetivo dessa pesquisa foi avaliar o perfil motor de crianças com Transtorno do Espectro Autista e comparar com a idade cronológica. Foram avaliadas crianças de dois a onze anos com diagnostico de Transtorno do Espectro Autista. A avaliação foi realizada por meio da Escala de Desenvolvimento Motor (EDM). Para análise das variáveis estudadas foi utilizado o teste de Kolmogorov-Smirnov para normatização e o teste t-Student para a comparação entre as variáveis numéricas, idade motora geral (IMG) e idade cronológica (IC). Adotou-se, para o teste o nível de significância de 5% de probabilidade para a rejeição da hipótese de nulidade. Participaram da coleta 14 crianças com diagnóstico de Transtorno do Espectro Autista, com idade média de 4,9 anos ± 1,6 anos. A média obtida de idade motora geral (IMG) foi de 35,7 meses e a média de idade cronológica (IC) foi de 66,7, sendo significativamente inferior à idade motora geral em comparação com a idade cronológica. Com relação aos domínios comtemplados pela EDM, não houve relevância estatisticamente significativa, porém, os domínios estão abaixo da média normativa estabelecida pela EDM (89-80), destacando a linguagem que se apresentou muito inferior, tendo média de 18,9. Os dados indicaram que as crianças avaliadas estão abaixo da média normativa do índice de desenvolvimento motor cronológico. Isso ocorre devido ao aumento no tempo de latência de resposta no Transtorno do Espectro Autista prejudicando seu sequenciamento motor e reduzindo as adaptações motoras necessárias. As perturbações motoras leves e moderadas podem passar despercebidas pelos profissionais que acompanham crianças com Transtorno do Espectro Autista, portanto, o tratamento é postergado e só ocorre em casos que as alterações se tornam graves e prejudicam o desempenho escolar e social da criança. Crianças diagnosticadas com o Transtorno Global do Desenvolvimento apresentam desempenho psicomotor inferior ao esperado para idade cronológica.

Gender Difference in the Association Between Executive Function and Autistic Traits in Typically Developing Children.

Autistic traits and executive function (EF) were assessed in 413 typically developing children aged 6-9years. The children were divided into the high- autistic-trait (HAT) and low-autistic-trait (LAT) groups based on their total autistic traits. Results suggested that there were gender differences in specific autistic traits in children with LAT. There were gender-specific associations between EF and autistic traits in children with HAT: the set shifting of EF predicted difficulties in social awareness in boys; whereas all the EF components predicted difficulties in social communication and social cognition in girls. These findings may have implications for developing customized interventions that are targeted at specific autistic deficits in males and females.

Prior Knowledge, Episodic Control and Theory of Mind in Autism: Toward an Integrative Account of Social Cognition.

Over the last 30 years, research has explored theory of mind (ToM), the ability to attribute mental states to oneself and to others. Work on ToM in typical and atypical populations has shed light on the neurocognitive mechanisms underlying social understanding and interaction. The ToM hypothesis has long been regarded as one comprehensive explanation of the severe cognitive and behavioral impairments encountered by individuals with autism. However, high-functioning individuals can often pass both first-order and second-order false belief tasks using cognitive compensation strategies. To provide more sensitive measures of mental state attribution abilities, researchers have introduced more difficult, “advanced” theory of mind tasks. In this article, we argue that in attempting to bypass compensation strategies, these new advanced ToM tasks, such as the Faux Pas and the Strange Stories tasks, impose cognitive demands beyond those specific to the domain of ToM. We then provide an integrative account of social deficits in autism that takes into account several distinct components of mental state understanding, including both general cognitive capacities and processes specific to ToM. We argue that a number of related cognitive abilities, including episodic cognitive control and inferencing from prior knowledge, are necessary to understand how both people with autism and typical development navigate challenging, real-life social situations.

MICROBIAL CONSORTIUM AND OXYTOCINE IN THE SOCIAL BEHAVIOR OF CHILDREN WITH AUTISM SPECTRUM DISORDERS

Aim. To assess the structure of the intestinal microbial consortium and the level of oxytocin in blood plasma in the context of severe social insufficiency in children with autism spectrum disorders. Materials and methods. 44 children with autism spectrum disorders were divided into two groups: 23 children with no signs of social contact and 21 people with preserved social contact. The comparison group was consisted of 39 typically developing children of the appropriate gender and age. The structure and quantity of microorganisms of the small intestine was determined with the help of specific lipid markers in peripheral blood by gas chromatography-mass spectrometry of microbial markers. The concentration of oxytocin was assessed in plasma by the method of ELISA. Results. Normally, the biochemical signals of the ecological system (the host-associated microbial consortium and the neuropeptide-oxytocin) work in the general context of the socialization of the meta-organism. However, an imbalance of the system (disease - autism spectrum disorders) can lead to change context and social insufficiency. Conclusion. Research in this direction will help, as we believe, to understand of the mechanisms underlying social deficits in autism, which will allow us to determine the ways of their correction.

Gamma Oscillation Dysfunction in mPFC Leads to Social Deficits in Neuroligin 3 R451C Knockin Mice

Neuroligins (NLs) are critical for synapse formation and function. NL3 R451C is an autism-associated mutation. NL3 R451C knockin (KI) mice exhibit autistic behavioral abnormalities, including social novelty deficits. However, neither the brain regions involved in social novelty nor the underlying mechanisms are clearly understood. Here, we found decreased excitability of fast-spiking interneurons and dysfunction of gamma oscillation in the medial prefrontal cortex (mPFC), which contributed to the social novelty deficit in the KI mice. Neuronal firing rates and phase-coding abnormalities were also detected in the KI mice during social interactions. Interestingly, optogenetic stimulation of parvalbumin interneurons in the mPFC at 40Hz nested at 8Hz positively modulated the social behaviors of mice and rescued the social novelty deficit in the KI mice. Our findings suggest that gamma oscillation dysfunction in the mPFC leads to social deficits in autism, and manipulating mPFC PV interneurons may reverse the deficits in adulthood.

Missing the egocentric spatial reference: a blank on the map.

Egocentric (self-centered) and allocentric (viewpoint independent) representations of space are essential for spatial navigation and wayfinding. Deficits in spatial memory come with age-related cognitive decline, are marked in mild cognitive impairment (MCI) and Alzheimer's disease (AD), and are associated with cognitive deficits in autism. In most of these disorders, a change in the brain areas engaged in the spatial reference system processing has been documented. However, the spatial memory deficits observed during physiological and pathological aging are quite different. While patients with AD and MCI have a general spatial navigation impairment in both allocentric and egocentric strategies, healthy older adults are particularly limited in the allocentric navigation, but they can still count on egocentric navigation strategy to solve spatial tasks. Therefore, specific navigational tests should be considered for differential diagnosis between healthy and pathological aging conditions. Finally, more research is still needed to better understand the spatial abilities of autistic individuals.

Impaired Value Learning for Faces in Preschoolers With Autism Spectrum Disorder

One of the common findings in autism spectrum disorder (ASD) is limited selective attention toward social objects, such as faces. Evidence from both human and nonhuman primate studies suggests that selection of objects for processing is guided by the appraisal of object values. We hypothesized that impairments in selective attention in ASD may reflect a disruption of a system supporting learning about object values in the social domain. We examined value learning in social (faces) and nonsocial (fractals) domains in preschoolers with ASD (n= 25) and typically developing (TD) controls (n= 28), using a novel value learning task implemented on a gaze-contingent eye-tracking platform consisting of value learning and a selective attention choice test. Children with ASD performed more poorly than TD controls on the social value learning task, but both groups performed similarly on the nonsocial task. Within-group comparisons indicated that value learning in TD children was enhanced on the social compared to the nonsocial task, but no such enhancement was seen in children with ASD. Performance in the social and nonsocial conditions was correlated in the ASD but not in the TD group. The study provides support for a domain-specific impairment in value learning for faces in ASD, and suggests that, in ASD, value learning in social and nonsocial domains may rely on a shared mechanism. These findings have implications both for models of selective social attention deficits in autism and for identification of novel treatment targets.

Social cognition in autism: Face tuning

Faces convey valuable information for social cognition, effective interpersonal interaction, and non-verbal communication. Face perception is believed to be atypical in autism, but the origin of this deficit is controversial. Dominant featural face encoding is suggested to be responsible for face tuning scarcity. Here we used a recently developed Face-n-Food paradigm for studying face tuning in individuals with autistic spectrum disorders (ASD). The key benefit of these images is that single components do not explicitly trigger face processing. In a spontaneous recognition task, adolescents with autism and typically developing matched controls were presented with a set of Face-n-Food images in different degree resembling a face (slightly bordering on the Giuseppe Arcimboldo style). The set of images was shown in a predetermined order from the least to most resembling a face. Thresholds for recognition of the Face-n-Food images as a face in ASD individuals were substantially higher than in typically developing controls: they did not report seeing a face on the images, which controls easily recognized as a face, and gave overall fewer face responses. This outcome not only lends support to atypical face tuning, but provides novel insights into the origin of face encoding deficits in autism.

Speech-specific categorical perception deficit in autism: An Event-Related Potential study of lexical tone processing in Mandarin-speaking children

Recent studies reveal that tonal language speakers with autism have enhanced neural sensitivity to pitch changes in nonspeech stimuli but not to lexical tone contrasts in their native language. The present ERP study investigated whether the distinct pitch processing pattern for speech and nonspeech stimuli in autism was due to a speech-specific deficit in categorical perception of lexical tones. A passive oddball paradigm was adopted to examine two groups (16 in the autism group and 15 in the control group) of Chinese children’s Mismatch Responses (MMRs) to equivalent pitch deviations representing within-category and between-category differences in speech and nonspeech contexts. To further examine group-level differences in the MMRs to categorical perception of speech/nonspeech stimuli or lack thereof, neural oscillatory activities at the single trial level were further calculated with the inter-trial phase coherence (ITPC) measure for the theta and beta frequency bands. The MMR and ITPC data from the children with autism showed evidence for lack of categorical perception in the lexical tone condition. In view of the important role of lexical tones in acquiring a tonal language, the results point to the necessity of early intervention for the individuals with autism who show such a speech-specific categorical perception deficit.

Mice lacking GRIP1/2 show increased social interactions and enhanced phosphorylation at GluA2-S880

Glutamate receptor interacting proteins 1 and 2 (GRIP1/2) play an important role in regulating synaptic trafficking of AMPA receptor 2/3 (GluA2/3) and synaptic strength. Gain-of-function GRIP1 mutations are implicated in social behavioral deficits in autism. To study mechanisms of Grip1/2-mediated AMPA signaling in the regulation of social behaviors, we performed social behavioral testing on neuron-specific Grip1/2-double knockout (DKO) and wild type (WT) mice that are matched for age, sex, and strain background. We determined the expression profile of key signaling proteins in AMPAR, mGluR, mTOR, and GABA pathways in frontal cortex, striatum, and cerebellum of DKO mice. Compared to WT mice, DKO mice show increased sociability in a modified three-chamber social behavioral test [mean±sem for interaction time in seconds; WT: 44.0±5.0; n=10; DKO: 81.0±9.0; n=9; two factor repeated measures ANOVA: F(1,37)=14.45; p<0.01 and planned t-test; p<0.01] and in a dyadic male–male social interaction test (mean±sem for total time in seconds: sniffing, WT-WT, 18.9±1.1; WT-DKO, 42.5±2.1; t-test: p<0.001; following, WT-WT, 7.7±0.72; WT-DKO,14.4±1.8; t-test: p<0.001). Immunoblot studies identified an increase in phosphorylation at GluA2-Serine 880 (GluA2-pS880) in frontal cortex (mean±sem; WT: 0.69±0.06, n=5; DKO: 0.96±0.06, n=6; t-test; p<0.05) and reduced GABAβ3 expression in striatum (mean±sem; WT: 1.16±0.04, n=4; DKO: 0.95±0.06, n=4; t-test; p<0.05) in DKO mice. GluA2-S880 phosphorylation is known to regulate GluA2synaptic recycling, AMPA signaling strength and plasticity. GABAβ3 has been implicated in the etiology and pathogenesis in autism. These data support an important role of Grip1/2-mediated AMPA signaling in regulating social behaviors and disturbance of glutamate- and GABA-signaling in specialized brain regions in autism-related social behavioral deficits.

Cortical interactions during the resolution of information processing demands in autism spectrum disorders

IntroductionOur flexible and adaptive interactions with the environment are guided by our individual representation of the physical world, estimated through sensation and evaluation of available information against prior knowledge. When linking sensory evidence with higher‐level expectations for action, the central nervous system (CNS) in typically developing (TD) individuals relies in part on distributed and interacting cortical regions to communicate neuronal signals flexibly across the brain. Increasing evidence suggests that the balance between levels of signal and noise during information processing may be disrupted in individuals with Autism Spectrum Disorders (ASD).MethodsParticipants with and without ASD performed a visuospatial interference task while undergoing functional Magnetic Resonance Imaging (fMRI). We empirically estimated parameters characterizing participants’ latencies and their subtle fluctuations (noise accumulation) over the 16‐min scan. We modeled hemodynamic activation and used seed‐based analyses of neural coupling to study dysfunction in interference‐specific connectivity in a subset of ASD participants who were nonparametrically matched to TD participants on age, male‐to‐female ratio, and magnitude of movement during the scan.ResultsStochastic patterns of response fluctuations reveal significantly higher noise‐to‐signal levels and a more random and noisy structure in ASD versus TD participants, and in particular ASD adults who have the greatest clinical autistic deficits. While individuals with ASD show an overall weaker modulation of interference‐specific functional connectivity relative to TD individuals, in particular between the seeds of Anterior Cingulate Cortex (ACC) and Inferior Parietal Sulcus (IPS) and the rest of the brain, we found that in ASD, higher uncertainty during the task is linked to increased interference‐specific coupling between bilateral anterior insula and prefrontal cortex.ConclusionsSubtle and informative differences in the structure of experiencing information exist between ASD and TD individuals. Our findings reveal in ASD an atypical capacity to apply previously perceived information in a manner optimal for adaptive functioning, plausibly revealing suboptimal message‐passing across the CNS.

Piecing together a different picture: A host of new studies on autism have begun decoding the longstanding puzzle of its causes.

“A developmental disability that hinders the normal functioning of the brain, affecting, in varying degrees, communication skills and social interaction. Repetitive behaviours, and different ways of learning, paying attention, or reacting to things are often distinctive signs”. This standard definition of autism fails to describe the complexity of a condition that ranges in its manifestations from severe intellectual impairment to superior cognitive skills, like in the Asperger syndrome. To comprise such diversity, autism disorders are now covered under the umbrella term “autism spectrum disorder” (ASD). In most cases, ASD manifests during the first 5 years of life, with boys significantly more likely to be diagnosed than girls. ASD usually goes together with several other problems that frequently include anxiety, sleep disorders, or epilepsy. No cure exists; treatment, such as speech therapy, just attempts to alleviate specific deficits of autistic patients. > Nothing is simple in autism. Even the real number of people affected is uncertain. Nothing is simple in autism. Even the real number of people affected is uncertain. The US CDC estimates that about 1 in 68 (or 1.5%) of children in the USA are living with ASD (http://www.cdc.gov/ncbddd/autism/data.html). The WHO has a more conservative estimate, last revised in January this year, of 1 in 160 children, based on a larger set of epidemiological surveys (http://www.who.int/mediacentre/factsheets/autism-spectrum-disorders/en/). Needless to say, most studies were conducted in developed countries, and the prevalence of ASD in many low‐ and middle‐income countries remains largely unknown. > Along the years, many potential causes have been indicated, including genetic and environmental factors, exposure to toxins during pregnancy, wide gaps between parent ages, and so on Although the general consensus is that prevalence rates are increasing globally, this point is debated too. Some analyses indicate that a large percentage of the increase in ASD owes to improved awareness and …