Form Of Autism Research Articles

Visual social attention in SYNGAP1-related intellectual disability.

SYNGAP1-ID is a neurodevelopmental disorder caused by a mutation of the SYNGAP1 gene. Characterized by moderate to severe developmental delay, it is associated with several physical and behavioral issues as well as additional diagnoses, including autism. However, it is not known whether social cognitive differences seen in SYNGAP1-ID are similar to those previously identified in idiopathic or other forms of autism. This study therefore investigated visual social attention in SYNGAP1-ID. Eye movements were recorded across three passive viewing tasks (face scanning, pop-out, and social preference) of differing social complexity in 24 individuals with SYNGAP1-ID and 12 typically developing controls. We found that SYNGAP1-ID participants looked at faces less than the controls, and when they did look at faces, they had less time looking at and fewer fixations to the eyes. For the pop-out task, where social and nonsocial objects (Phone, car, face, bird, and face-noise) were presented in an array, those with SYNGAP1-ID spent significantly less time looking at the phone stimulus as well as fewer fixations to the face compared with the typically developing controls. When looking at two naturalistic scenes side by side, one social in nature (e.g., with children present) and the other not, there were no differences between the SYNGAP1-ID group and typically developing controls on any of the examined eye tracking measures. This study provides novel findings on the social attention of those with SYNGAP1-ID and helps to provide further evidence for using eye tracking as an objective measure of the social phenotype in this population in future clinical trials.

Особенности речи и устного дискурса при детском аутизме: описание случая спонтанного билингвизма. Часть II: психолингвистическое исследование

<p style="text-align: justify;"><strong>Objectives. </strong>Pronounced disharmony in verbal communication development is considered a typical developmen­tal feature in infantile autism, however, its manifestations and mechanisms have not yet been studied enough; extremely little is known about the qualitative features of speech development and the psycholinguistic char­acteristics of the language abilities of such children. A dissociation between the semantic-pragmatic and struc­tural-functional components of language development has been reported; however, this feature has significant individual variability in different forms of autism. The aim of the current paper is to introduce a longitudinal study of the speech development in a child with autism accompanied by the phenomenon of spontaneous bilin­gualism in a monolingual family.</p> <p style="text-align: justify;"><strong>Methods. </strong>A case of a Lithuanian monolingual boy with early childhood autism is presented, who at the age of 4 years independently began to learn English, which resulted by the end of preschool age in the unbalanced bilingualism with a preference for L2. Longitudinal follow-up included 3 complex clinical examinations of the intellectual and language abilities (at 4, 6 and 8 years) and a psycholinguistic study of language skills in Lithuanian and English at the age of 7years. A battery of tests for assessing grammar, impressive and expres­sive vocabulary, and skills of personal discourse (story-telling and participating in dialogue-reasoning) was employed.</p> <p style="text-align: justify;"><strong>Results. </strong>In both languages, a deficiency in the pragmatic competence of story-telling and participating in dialogue-reasoning was revealed; however, lexical and grammatical errors occurred mainly in the native (Lithuanian) language. The study evidenced a deficit of verb expressive vocabulary, especially in Lithuanian language. Comprehension of complex grammatical constructions was impaired in the Lithuanian language to a greater extent than in English. To sum up, the results evidenced a partial compensation for the structural and functional impairment, but the persistence of a deficit in the pragmatics of speech.</p> <p style="text-align: justify;"><strong>Conclusions. </strong>The case study illustrates the special nature of speech development in a child with autism and a unique phenomenon of spontaneous bilingualism in a monolingual family.</p>

Integrin β3 regulates apical dendritic morphology of pyramidal neurons throughout hippocampal CA3.

In excitatory hippocampal pyramidal neurons, integrin β3 is critical for synaptic maturation and plasticity in vitro. Itgb3 is a potential autism susceptibility gene that regulates dendritic morphology in the cerebral cortex in a cell-specific manner. However, it is unknown what role Itgb3 could have in regulating hippocampal pyramidal dendritic morphology in vivo, a key feature that is aberrant in many forms of autism and intellectual disability. We found that Itgb3 mRNA is expressed in the stratum pyramidale of CA3. We examined the apical dendritic morphology of CA3 hippocampal pyramidal neurons in conditional Itgb3 knockouts and controls, utilizing the Thy1-GFP-M line. We fully reconstructed the apical dendrite of each neuron and determined each neuron's precise location along the dorsoventral, proximodistal, and radial axes of the stratum pyramidale. We found a very strong effect for Itgb3 expression on CA3 apical dendritic morphology: neurons from conditional Itgb3 knockouts had longer and thinner apical dendrites than controls, particularly in higher branch orders. We also assessed potential relationships between pairs of topographic or morphological variables, finding that most variable pairs were free from any linear relationships to each other. We also found that some neurons from controls, but not conditional Itgb3 knockouts, had a graded pattern of overall diameter along the dorsoventral and proximodistal axes of the stratum pyramidale of CA3. Taken together, Itgb3 is essential for constructing normal dendritic morphology in pyramidal neurons throughout CA3.

Stem Cell Treatment of Autism Spectrum Disorders

Autism is a spectrum of neurodevelopmental disorders. It appears differently in all individuals with ASDs and has recently become popular in research. There are many suspected genetic causes of autism, but no cure has been proven to work to treat the disorder. Stem cells have been studied for their potential role in treating ASDs. The most promising results have come from studies utilizing MSCs or hESCs. Experiments have shown that using these stem cells can reduce the severity of autism and increase the quality of life. Stem cells have also been used to model different forms of autism, including Rett Syndrome and Fragile X Syndrome. The most common stem cells used for modeling autism are iPSCs, which can retain the original genetics of the patient it was derived from. By studying autism precisely how it appears in the body, novel drug therapies and treatments can be designed. There are moral considerations that need to be taken into account when studying novel therapies for autism. The most common participants in these studies are children. This population needs to be protected, and researchers should keep their best interests in mind. Also, scientists should acknowledge their work's impact on the general population and hold each other accountable for the work they release.

Impaired synaptic plasticity in an animal model of autism exhibiting early hippocampal GABAergic-BDNF/TrkB signaling alterations

In Neurodevelopmental Disorders, alterations of synaptic plasticity may trigger structural changes in neuronal circuits involved in cognitive functions. This hypothesis was tested in mice carrying the human R451C mutation of Nlgn3 gene (NLG3R451C KI), found in some families with autistic children. To this aim, the spike time dependent plasticity (STDP) protocol was applied to immature GABAergic Mossy Fibers (MF)-CA3 connections in hippocampal slices from NLG3R451C KI mice. These animals failed to exhibit STD-LTP, an effect that persisted in adulthood when these synapses became glutamatergic. Similar results were obtained in mice lacking the Nlgn3 gene (NLG3 KO mice), suggesting a loss of function. The loss of STD-LTP was associated with a premature shift of GABA from the depolarizing to the hyperpolarizing direction, a reduced BDNF availability and TrkB phosphorylation at potentiated synapses. These effects may constitute a general mechanism underlying cognitive deficits in those forms of Autism caused by synaptic dysfunctions.

Fonctionnements autistiques et perspectives psychopathologiques sur le devenir des personnes autistes

ObjectivesPsychoanalytical and other theories of autism are mainly based on infantile clinical observation. Considering this, the perspective of the personal evolution of autistic persons during their teenage years and adulthood opens questions leading to a necessary reassessment of theoretical knowledge. Over the last decade, our understanding of autistic pathologies has increasingly underlined the importance of sensory elements in their symptomatic expression. The main objective of this theoretical reflection is to formulate new theoretical suggestions to help better understand the evolutions of autistic persons. Notably, this includes hypotheses allowing us to articulate the psychic functioning of autistic persons to other psychopathological functioning. MethodThis research is based on autobiographical writing by autistic persons, leading to a phenomenological point of view, which will be completed with elements of clinical experience. This corpus of knowledge offers insight into dismantling, stimming, and sensory pursuit, allowing us to better understand the peculiar forms of the use of the sensorial in the psychic functioning of autistic subjects. It will refer to existing psychoanalytical writing on autism, thereby suggesting a new psychopathological understanding of the archaic dimension made visible by autistic pathologies. ResultsDifferences between different forms of autism and psychosis are interrogated, in order to further understanding of clinical situations where this distinction is less evident. Autobiographical writing by autistic persons promotes understanding of the ways in which the sensory dimension plays a specific part in psychic functioning. What psychic processes are present in the sensory part of mental functioning of those subjects is theorized. Focusing on self-stimulatory behavior and sensory pursuit as they are seen in autism, it is suggested that psychic functioning builds itself with these sensory elements, thus stabilizing the psychic apparatus. The notion of autistic functioning is introduced to explain subjects’ reliance on the sensorial register as a stabilizer of the psychic apparatus. Psychic drives invest sensory sensations which are preorganized by the Id in order to become a perception. Then, these particular uses of sensory elements and perception find a way to persist in the subject's psychic functioning in diverse forms. This leads to a persistence of archaic functioning in the psyche that also can invest in other functioning. Three outlooks are explored. First, that autistic pathologies can develop in many ways, including evolutions where psychic functioning is closer to what exists in psychotic functioning. Then, how some psychotic subjects can make use of autistic functioning to help them deal with splitting anxiety. Lastly, autistic functioning can also punctually exist in certain types of trauma, opening the question of its existence outside of psychosis and autism. DiscussionThe notion of autistic functioning makes it clears how some archaic functioning, as seen un autistic persons, can maintain itself throughout subjects’ development. In the meantime, other psychic functioning appears and develops during teenage years and adulthood. Furthermore, this notion opens the question of differential diagnosis with psychosis and the possibility for autistic functioning to exist outside of autism. ConclusionsThe notion of autistic functioning leads to another way of thinking about the personal evolution of autistic persons as they get older. It, nonetheless, will require further reflection, particularly as regards evaluating its clinical relevance, as well as its usefulness for differential diagnosis.

AUTISM AND CREATIVITY: A SOCIAL ROBOTICS APPLICATION

This paper focuses on the relationship of genius with certain forms of autism. It synthesizes some results of two ongoing research activities. The first one concerns the investigation of creativity and the arts in the digital age, while the second an educational experience to support the socialization of people with Autism Spectrum Disorder.The educational experience was based on storytelling, drama, and programmable toy robots.Our research emerged that low functioning autistic people may exhibit creative attitudes, but the creativity of educators has a crucial role in stimulating their creativity.

Этапное лечение расстройств аутистического спектра, ассоциированных с генетическим дефицитом фолатного цикла

В статье рассмотрено этапное лечение детей с расстройствами аутистического спектра, ассоциированными с генетическим дефицитом фолатного цикла, в свете новых открытий в патогенезе заболевания. Предложено разделить рекомендуемые терапевтические вмешательства на 3 последовательных этапа: противомикробное/противовирусное лечение, иммунотерапия при помощи в/в иммуноглобулина, нейрореабилитация с использованием инновационных медикаментозных средств и междисциплинарной немедикаментозной помощи. Особая форма аутистических расстройств, связанных с генетическим дефицитом фолатного цикла, в отличие от других генетических форм аутизма, является потенциально курабельной болезнью, и этапная стратификация терапевтических подходов позволяет добиться больших успехов в преодолении инвалидизирующих психических нарушений, которые ранее представлялись неизлечимыми.

Consistent, convergent pathways link two forms of autism

Consistent, convergent pathways link two forms of autism

Different forms of autism have opposite problems with brain precursor cells

Different forms of autism have opposite problems with brain precursor cells

A New Autism as The Next Pandemic: How Christian Education Eliminating Nomophobia

The world is grappling with the Covid-19 pandemic. This precarious situation forced adjustments in every aspect of human life, not least in the field of education. We were facing a twin pandemic, which is damaging to physical health as well as mental health. This study aimed to analyze the influence of fatherlessness on nomophobia among Christian students in Indonesia. This is a quantitative research with survey methods. All participants (200 students) completed a battery of questioannaires assessing predictor and outcome variables related to nomophobia The result of the analysis revealed that fatherlesness condition had a strong correlation with nomophobia, a new form of autism that will be the next pandemic. This can be eliminated by restoring parental function in the family.

Experience in the use of transcranial micro polarization in children with autism spectrum disorders

Introduction. Autism is a disorder characterized by social interaction disorders, social-emotional reciprocity, responses to other people’s emotions, social use of speech skills, lack of modulations of behavior under the social situation, and limited interest stereotypes. The comprehensive approach using medical and psychological correction with physical methods of influence provides the best result in treating and rehabilitating children with autism. The original study examined the effects of transcranial micro polarization (TCMP) on the dynamics of autistic disorders. TCMP is a modern treatment method consisting of a directed polarizing impact of a low-power DC on specific brain areas. Materials and methods. There were observed 25 children aged from 2 years five months to 6 years with varying degrees of severity of autism spectrum disorders (ASD). For the study, three groups were identified according to the corresponding clinical diagnoses: Childhood autism, Atypical autism, and Other general developmental disorders. The vast majority of children from the first two groups had an intellectual disability of varying severity. The TCMP method was used to assess the technique’s effectiveness, the CARS diagnostic scale and the ATEK test. Results. At the end of the course, with the use of TCMP in all the analyzed groups, there was a shift towards a milder degree of autistic disorders. The most significant positive effect was recorded in children with mild forms of autism in the group of other general developmental disorders due to the initially higher level of development in this group. Conclusion. The results obtained demonstrate the effectiveness of TCMP in ASD children. According to the results of the study, the positive effect of this method was revealed in the form of reducing the severity of autistic disorders.

Oxytocin and vasopressin: the social networking buttons of the body

Neurotransmitters play the role of electrochemical signalling molecules which are essential for suitable brain functioning. Their dysfunction causes several mental and health disorders. Neurotransmitters are present at a very low concentration in the nervous system and they are mixed with many other biochemical molecules. The precise detection and nursing of these molecules are pretty decisive in brain studies. This mini-review portrays the research on oxytocin and vasopressin as an exemplar for exploring the social neuroscience as the subject of social neuroscience has decisively explored the complex territory between perception and action. These neuropeptides, oxytocin and vasopressin are evolutionarily extremely conserved mediators in order to regulate the complex social cognition and behaviour. They play significant role in social interactions, in maternal care and closeness, development of general trust and cooperation, controlling of labor and breastfeeding, regulation of blood pressure, social recognition, sexual behaviours and response to stress. They find applications for several treatment approaches in mental disorders in the form of autism, borderline personality disorder, social anxiety disorder and schizophrenia.

Features of teaching swimming to children of primary school age with autism spectrum disorder

The article presents an analysis of the peculiarities of teaching swimming to children of primary school age with autism spectrum disorder. The study was conducted on the basis of the sports complex “Burevestnik” in Kazan. According to the results of testing on the scale of assessment of the degree of autism of children, a group of boys aged 9-10 years was formed. In four children, the degree of autism is not expressed and moderately pronounced, in one child-a severe form of autism. At the time of the examination, the children did not know how to swim. Classes on the water were held for six months 3 times a week for 40 minutes. The children trained using the author’s equipment – special boards with an associative character (a fish with bubbles, a whale with a fountain, a dolphin, a frog, a turtle, a rocket). The size of the swimming board remained standard, 32x25cm. The development of the supporting device was due to the need to eliminate the inadequate response to various sensory stimuli, such as touching strangers or tactile contact with unfamiliar objects and textures, as well as to obtain positive associations and mental images for the successful development of a new exercise. At the end of six months of classes, all children with autism spectrum disorder have mastered swimming training according to the indicators: 1) immersion in water with exhalation in water, 2) sliding on the chest with the movement of the legs, 3) sliding on the chest with the movement of the legs and performing proper breathing. The study was determined by the ability to use boards to swim copyright form associative nature.

Intervention Models for The Pre-Integration of Children with ASD in Mainstream Education

The pathology of autism dates back to the 1900s, being framed within the broad sphere of neuropsychological conditions. So far, the autism spectrum disorder (ASD) has passed through various pathologies, from socio-emotional disorders to schizophrenic disorders. The clear distinction between childhood autism and childhood schizophrenia was only made in the early 1980s. ASD is one of the most common invasive developmental disorders; defined as a neurological condition characterised by a distortion in the overall development of a person, it affects 1 in 150 children and 4 to 5 boys per girl. The autistic triad brings together qualitative anomalies in social interactions (in verbal and nonverbal communication), restricted interests and stereotypes. The 1980s and 1990s highlight the role of behavioural therapy and the use of highly controlled learning environments as a primary treatment for the forms of autism and related conditions. Promising studies on the role of oxytocin or certain amino acids involved in neurotransmission, especially in regulating stress and its emotional consequences, are currently in progress. Until now, the two therapies have remained primordial along with physical therapy and speech therapy. The purpose of this paper is to present some of the means that can contribute to the pre-integration of children in mainstream education, being also a starting point for future applied research. At the same time, the paper is helpful for the parents of children with ASD, who are given the opportunity to work themselves in the absence of a specialist or financial possibilities.

Neuromarketing Highlights in How Asperger Syndrome Youth Perceive Advertising.

This study examines how advertising material and brands related to organizational communication are perceived by people with Asperger syndrome, a form of autism. The main objective of the study was to understand whether the perception of advertising differs between individuals with AS and a neurotypical population. Neuromarketing techniques were used to examine two key variables, attention and emotion, which were also measured by physiological and biometric variables. The results were compared with those of a control group from a neurotypical population; i.e., participants who had not been diagnosed with any type of developmental disorder. Commercial advertisements were the preferred material used in this research although social-themed advertisements were also included, some produced by commercial companies and others by institutional advertisers (NGOs and foundations). Qualitative techniques were also used to explain the observed phenomena. Data revealed significant differences between the two groups in their perception of advertising and organizational communication with respect to attention and emotion variables.

PKA and Ube3a regulate SK2 channel trafficking to promote synaptic plasticity in hippocampus: Implications for Angelman Syndrome

The ubiquitin ligase, Ube3a, plays important roles in brain development and functions, since its deficiency results in Angelman Syndrome (AS) while its over-expression increases the risk for autism. We previously showed that the lack of Ube3a-mediated ubiquitination of the Ca2+-activated small conductance potassium channel, SK2, contributes to impairment of synaptic plasticity and learning in AS mice. Synaptic SK2 levels are also regulated by protein kinase A (PKA), which phosphorylates SK2 in its C-terminal domain, facilitating its endocytosis. Here, we report that PKA activation restores theta burst stimulation (TBS)-induced long-term potentiation (LTP) in hippocampal slices from AS mice by enhancing SK2 internalization. While TBS-induced SK2 endocytosis is facilitated by PKA activation, SK2 recycling to synaptic membranes after TBS is inhibited by Ube3a. Molecular and cellular studies confirmed that phosphorylation of SK2 in the C-terminal domain increases its ubiquitination and endocytosis. Finally, PKA activation increases SK2 phosphorylation and ubiquitination in Ube3a-overexpressing mice. Our results indicate that, although both Ube3a-mediated ubiquitination and PKA-induced phosphorylation reduce synaptic SK2 levels, phosphorylation is mainly involved in TBS-induced endocytosis, while ubiquitination predominantly inhibits SK2 recycling. Understanding the complex interactions between PKA and Ube3a in the regulation of SK2 synaptic levels might provide new platforms for developing treatments for AS and various forms of autism.

Effectiveness of Noise-Attenuating Headphones on Physiological Responses for Children With Autism Spectrum Disorders.

Objective: The purpose of this study was to evaluate the proof of concept of an intervention to decrease sympathetic activation as measured by skin conductivity (electrodermal activity, EDA) in children with an autism spectrum disorder (ASD) and auditory hypersensitivity (hyperacusis). In addition, researchers examined if the intervention provided protection against the negative effects of decibel level of environmental noises on electrodermal measures between interventions. The feasibility of implementation and outcome measures within natural environments were evaluated.Method: A single-subject multi-treatment design was used with six children, aged 8–16 years, with a form of Autism (i.e., Autism, PDD-NOS). Participants used in-ear (IE) and over-ear (OE) headphones for two randomly sequenced treatment phases. Each child completed four phases: (1) a week of baseline data collection; (2) a week of an intervention; (3) a week of no intervention; and (4) a week of the other intervention. Empatica E4 wristbands collected EDA data. Data was collected on 16–20 occasions per participant, with five measurements per phase.Results: Separated tests for paired study phases suggested that regardless of intervention type, noise attenuating headphones led to a significance difference in both skin conductance levels (SCL) and frequency of non-specific conductance responses (NS-SCRs) between the baseline measurement and subsequent phases. Overall, SCL and NS-SCR frequency significantly decreased between baseline and the first intervention phase. A protective effect of the intervention was tested by collapsing intervention results into three phases. Slope correlation suggested constant SCL and NS-SCR frequency after initial use of the headphones regardless of the increase in environmental noises. A subsequent analysis of the quality of EDA data identified that later phases of data collection were associated with better data quality.Conclusion: Many children with ASD have hypersensitivities to sound resulting in high levels of sympathetic nervous system reactivity, which is associated with problematic behaviors and distress. The findings of this study suggest that the use of noise attenuating headphones for individuals with ASD and hyperacusis may reduce sympathetic activation. Additionally, results suggest that the use of wearable sensors to collect physiological data in natural environments is feasible with established protocols and training procedures.

Audiogenic Seizures in the Fmr1 Knock-Out Mouse Are Induced by Fmr1 Deletion in Subcortical, VGlut2-Expressing Excitatory Neurons and Require Deletion in the Inferior Colliculus.

Fragile X syndrome (FXS) is the most common form of inherited intellectual disability and the leading monogenetic cause of autism. One symptom of FXS and autism is sensory hypersensitivity (also called sensory over-responsivity). Perhaps related to this, the audiogenic seizure (AGS) is arguably the most robust behavioral phenotype in the FXS mouse model-the Fmr1 knock-out (KO) mouse. Therefore, the AGS may be considered a mouse model of sensory hypersensitivity. Hyperactive circuits are hypothesized to underlie dysfunction in a number of brain regions in patients with FXS and Fmr1 KO mice, and the AGS may be a result of this. But the specific cell types and brain regions underlying AGSs in the Fmr1 KO are unknown. We used conditional deletion or expression of Fmr1 in different cell populations to determine whether Fmr1 deletion in those cells was sufficient or necessary, respectively, for the AGS phenotype in males. Our data indicate that Fmr1 deletion in glutamatergic neurons that express vesicular glutamate transporter 2 (VGlut2) and are located in subcortical brain regions is sufficient and necessary to cause AGSs. Furthermore, the deletion of Fmr1 in glutamatergic neurons of the inferior colliculus is necessary for AGSs. When we demonstrate necessity, we show that Fmr1 expression in either the larger population of VGlut2-expressing glutamatergic neurons or the smaller population of inferior collicular glutamatergic neurons-in an otherwise Fmr1 KO mouse-eliminates AGSs. Therefore, targeting these neuronal populations in FXS and autism may be part of a therapeutic strategy to alleviate sensory hypersensitivity.SIGNIFICANCE STATEMENT Sensory hypersensitivity in fragile X syndrome (FXS) and autism patients significantly interferes with quality of life. Audiogenic seizures (AGSs) are arguably the most robust behavioral phenotype in the FXS mouse model-the Fmr1 knockout-and may be considered a model of sensory hypersensitivity in FXS. We provide the clearest and most precise genetic evidence to date for the cell types and brain regions involved in causing AGSs in the Fmr1 knockout and, more broadly, for any mouse mutant. The expression of Fmr1 in these same cell types in an otherwise Fmr1 knockout eliminates AGSs indicating possible cellular targets for alleviating sensory hypersensitivity in FXS and other forms of autism.

Quantum-like behavior without quantum physics III : Logic and memory.

We employ some of the machinery developed in previous work to investigate the inferential and memory functions of quantum-like neural networks. We set up a logical apparatus to implement this in the form of a Gentzen sequent calculus which codifies some of the combinatory rules for the state spaces of the neuronal networks introduced earlier. We discuss memory storage in this context and along the way find formal proof that synchronicity promotes binding and storage. These results lead to an algorithmic fragment in calculus that simulates the memory function known as pattern completion. This claim is tested by noting that the failure of certain steps in the algorithm leads to memory deficits essentially identical to those found in such pathologies as Alzheimer's dementia, schizophrenia, and certain forms of autism. Moreover, a specific "power-of-two" wiring architecture and computational logic, which have been postulated and observed across many brain circuits, emerge spontaneously from our model. We draw conclusions concerning the possible nature of such mental processes qua computations.