Статті в журналах: "Neural mechanisms autism"

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Watts, Timothy John. "The Pathogenesis of Autism." Clinical medicine. Pathology 1 (January 2008): CPath.S1143. http://dx.doi.org/10.4137/cpath.s1143.

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Autism is well known as a complex developmental disorder with a seemingly confusing and uncertain pathogenesis. The definitive mechanisms that promote autism are poorly understood and mostly unknown, yet available theories do appear to focus on the disruption of normal cerebral development and its subsequent implications on the functional brain unit. This mini-review aims solely to discuss and evaluate the most prominent current theories regarding the pathogenesis of autism. The main conclusion is that although there is not a clear pathway of mechanisms directed towards a simple pathogenesis and an established link to autism on the symptomatic level; there are however several important theories (neural connectivity, neural migration, excitatory-inhibitory neural activity, dendritic morphology, neuroimmune; calcium signalling and mirror neurone) which appear to offer an explanation to how autism develops. It seems probable that autism's neurodevelopmental defect is ‘multi-domain’ in origin (rather than a single anomaly) and is hence distributed across numerous levels of study (genetic, immunopathogenic, etc.). A more definitive understanding of the pathogenesis could facilitate the development of better treatments for this complex psychiatric disorder.

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Mazefsky, Carla A., Amanda Collier, Josh Golt, and Greg J. Siegle. "Neural features of sustained emotional information processing in autism spectrum disorder." Autism 24, no. 4 (February 28, 2020): 941–53. http://dx.doi.org/10.1177/1362361320903137.

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Emotion dysregulation is common in autism spectrum disorder; a better understanding of the underlying neural mechanisms could inform treatment development. The tendency toward repetitive cognition in autism spectrum disorder may also increase susceptibility to perseverate on distressing stimuli, which may then increase emotion dysregulation. Therefore, this study investigated the mechanisms of sustained processing of negative information in brain activity using functional magnetic resonance imaging. We used an event-related task that alternated between emotional processing of personally relevant negative words, neutral words, and a non-emotional task. A priori criteria were developed to define heightened and sustained emotional processing, and feature conjunction analysis was conducted to identify all regions satisfying these criteria. Participants included 25 adolescents with autism spectrum disorder and 23 IQ-, age-, and gender-matched typically developing controls. Regions satisfying all a priori criteria included areas in the salience network and the prefrontal dorsolateral cortex, which are areas implicated in emotion regulation outside of autism spectrum disorder. Collectively, activity in the identified regions accounted for a significant amount of variance in emotion dysregulation in the autism spectrum disorder group. Overall, these results may provide a potential neural mechanism to explain emotion dysregulation in autism spectrum disorder, which is a significant risk factor for poor mental health. Lay abstract Many individuals with autism spectrum disorder struggle with emotions that are intense and interfering, which is referred to as emotion dysregulation. Prior research has established that individuals with autism may be more likely than individuals who are not autistic to have repetitive thoughts. It is possible that persistent thoughts about negative or distressing stimuli may contribute to emotion dysregulation in autism spectrum disorder. This study aimed to identify areas of the brain with evidence of persistent processing of negative information via functional magnetic resonance neuroimaging. We used a task that alternated between emotional processing of personally relevant negative words, neutral words, and a non-emotional task. Criteria were developed to define heightened and persistent emotional processing, and analyses were conducted to identify all brain regions satisfying these criteria. Participants included 25 adolescents with autism spectrum disorder and 23 typically developing adolescents who were similar to the autism spectrum disorder group in IQ, age, and gender ratios. Brain regions identified as having greater and continued processing following negative stimuli in the autism spectrum disorder group as compared with the typically developing group included the salience network and the prefrontal dorsolateral cortex. These areas have been previously implicated in emotion dysregulation outside of autism spectrum disorder. Collectively, brain activity in the identified regions was associated with parent-reported emotion dysregulation in the autism spectrum disorder group. These results help to identify a potential process in the brain associated with emotion dysregulation in autism spectrum disorder. This information may be useful for the development of treatments to decrease emotion dysregulation in autism spectrum disorder.

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Bertone, Armando, Laurent Mottron, Patricia Jelenic, and Jocelyn Faubert. "Motion Perception in Autism: A “Complex” Issue." Journal of Cognitive Neuroscience 15, no. 2 (February 1, 2003): 218–25. http://dx.doi.org/10.1162/089892903321208150.

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We present the first assessment of motion sensitivity for persons with autism and normal intelligence using motion patterns that require neural processing mechanisms of varying complexity. Compared to matched controls, our results demonstrate that the motion sensitivity of observers with autism is similar to that of nonautistic observers for different types of first-order (luminance-defined) motion stimuli, but significantly decreased for the same types of second-order (texture-defined) stimuli. The latter class of motion stimuli has been demonstrated to require additional neural computation to be processed adequately. This finding may reflect less efficient integrative functioning of the neural mechanisms that mediate visuoperceptual processing in autism. The contribution of this finding with regards to abnormal perceptual integration in autism, its effect on cognitive operations, and possible behavioral implications are discussed.

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4

Richey, J. Anthony, Cara R. Damiano, Antoinette Sabatino, Alison Rittenberg, Chris Petty, Josh Bizzell, James Voyvodic, et al. "Neural Mechanisms of Emotion Regulation in Autism Spectrum Disorder." Journal of Autism and Developmental Disorders 45, no. 11 (January 25, 2015): 3409–23. http://dx.doi.org/10.1007/s10803-015-2359-z.

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Mosner, Maya G., R. Edward McLaurin, Jessica L. Kinard, Shabnam Hakimi, Jacob Parelman, Jasmine S. Shah, Joshua Bizzell, et al. "Neural Mechanisms of Reward Prediction Error in Autism Spectrum Disorder." Autism Research and Treatment 2019 (July 1, 2019): 1–10. http://dx.doi.org/10.1155/2019/5469191.

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Few studies have explored neural mechanisms of reward learning in ASD despite evidence of behavioral impairments of predictive abilities in ASD. To investigate the neural correlates of reward prediction errors in ASD, 16 adults with ASD and 14 typically developing controls performed a prediction error task during fMRI scanning. Results revealed greater activation in the ASD group in the left paracingulate gyrus during signed prediction errors and the left insula and right frontal pole during thresholded unsigned prediction errors. Findings support atypical neural processing of reward prediction errors in ASD in frontostriatal regions critical for prediction coding and reward learning. Results provide a neural basis for impairments in reward learning that may contribute to traits common in ASD (e.g., intolerance of unpredictability).

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Failla, Michelle D., Estephan J. Moana-Filho, Greg K. Essick, Grace T. Baranek, Baxter P. Rogers, and Carissa J. Cascio. "Initially intact neural responses to pain in autism are diminished during sustained pain." Autism 22, no. 6 (May 17, 2017): 669–83. http://dx.doi.org/10.1177/1362361317696043.

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Pain assessments typically depend on self-report of the pain experience. Yet, in individuals with autism spectrum disorders, this can be an unreliable due to communication difficulties. Importantly, observations of behavioral hypo- and hyperresponsivity to pain suggest altered pain sensitivity in autism spectrum disorder. Neuroimaging may provide insight into mechanisms underlying pain behaviors. The neural pain signature reliably responds to painful stimulation and is modulated by other outside regions, affecting the pain experience. In this first functional magnetic resonance imaging study of pain in autism spectrum disorder, we investigated neural responses to pain in 15 adults with autism spectrum disorder relative to a typical comparison group (n = 16). We explored temporal and spatial properties of the neural pain signature and its modulators during sustained heat pain. The two groups had indistinguishable pain ratings and neural pain signature responses during acute pain; yet, we observed strikingly reduced neural pain signature response in autism spectrum disorder during sustained pain and after stimulus offset. The posterior cingulate cortex, a neural pain signature modulating region, mirrored this late signal reduction in autism spectrum disorder. Intact early responses, followed by diminished late responses to sustained pain, may reflect altered pain coping or evaluation in autism spectrum disorder. Evidence of a dichotomous neural response to initial versus protracted pain may clarify the coexistence of both hypo- and hyperresponsiveness to pain in autism spectrum disorder.

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7

Schmitz, Nicole, Katya Rubia, Therese van Amelsvoort, Eileen Daly, Anna Smith, and Declan G. M. Murphy. "Neural correlates of reward in autism." British Journal of Psychiatry 192, no. 1 (January 2008): 19–24. http://dx.doi.org/10.1192/bjp.bp.107.036921.

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BackgroundLack of social interaction, which is characteristically seen in people with autistic-spectrum disorder, may be caused by malfunctioning of the frontostriatal reward systems. However, no reported in vivo brain imaging studies have investigated reward mechanisms in autistic-spectrum disorder.AimsTo investigate functional brain activation during reward feedback in people with autistic-spectrum disorder and control individuals.MethodWe used event-related functional magnetic resonance imaging to examine the neural substrates of monetary reward in individuals with autistic-spectrum disorder and matched controls.ResultsWhen rewarded, individuals with autism compared with control individuals showed significantly greater brain activation in the left anterior cingulate gyrus. In addition, activation of this region was negatively correlated with social interaction as measured by the Autism Diagnostic Interview.ConclusionsIn people with autistic-spectrum disorder, achieving reward is associated with significant differences in the activation of areas known to be responsible for attention and arousal, and this may partially underpin some deficits in social behaviour.

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Colizzi, Marco, Riccardo Bortoletto, Rosalia Costa, Sagnik Bhattacharyya, and Matteo Balestrieri. "The Autism–Psychosis Continuum Conundrum: Exploring the Role of the Endocannabinoid System." International Journal of Environmental Research and Public Health 19, no. 9 (May 5, 2022): 5616. http://dx.doi.org/10.3390/ijerph19095616.

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Evidence indicates shared physiopathological mechanisms between autism and psychosis. In this regard, the endocannabinoid system has been suggested to modulate neural circuits during the early stage of neurodevelopment, with implications for both autism and psychosis. Nevertheless, such potential common markers of disease have been investigated in both autism and psychosis spectrum disorders, without considering the conundrum of differentiating the two groups of conditions in terms of diagnosis and treatment. Here, we systematically review all human and animal studies examining the endocannabinoid system and its biobehavioral correlates in the association between autism and psychosis. Studies indicate overlapping biobehavioral aberrancies between autism and schizophrenia, subject to correction by modulation of the endocannabinoid system. In addition, common cannabinoid-based pharmacological strategies have been identified, exerting epigenetic effects across genes controlling neural mechanisms shared between autism and schizophrenia. Interestingly, a developmental and transgenerational trajectory between autism and schizophrenia is supported by evidence that exogenous alteration of the endocannabinoid system promotes progression to inheritable psychosis phenotypes in the context of biobehavioral autism vulnerability. However, evidence for a diametral association between autism and psychosis is scant. Several clinical implications follow from evidence of a developmental continuum between autism and psychosis as a function of the endocannabinoid system dysregulation.

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Greene, Rachel K., Cara R. Damiano-Goodwin, Erin Walsh, Joshua Bizzell, and Gabriel S. Dichter. "Neural Mechanisms of Vicarious Reward Processing in Adults with Autism Spectrum Disorder." Autism Research and Treatment 2020 (March 21, 2020): 1–12. http://dx.doi.org/10.1155/2020/8014248.

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Previous studies examining the neural substrates of reward processing in ASD have explored responses to rewards for oneself but not rewards earned for others (i.e., vicarious reward). This omission is notable given that vicarious reward processing is a critical component of creating and maintaining social relationships. The current study examined the neural mechanisms of vicarious reward processing in 15 adults with ASD and 15 age- and gender-matched typically developing controls. Individuals with ASD demonstrated attenuated activation of reward-related regions during vicarious reward processing. Altered connectivity was also observed in individuals with ASD during reward receipt. These findings of altered neural sensitivity to vicarious reward processing may represent a mechanism that hinders the development of social abilities in ASD.

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10

Leite, Júlio Fernandes, and Umberto Euzebio. "Anormalidades da formação cerebral e os transtornos de desenvolvimento neural." STUDIES IN HEALTH SCIENCES 2, no. 1 (September 17, 2021): 2–23. http://dx.doi.org/10.54018/shsv2n1-001.

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Transtornos do desenvolvimento neural constituem um grupo bastante diverso de problemas identificáveis clinicamente, que decorrem de perturbações do desenvolvimento neurológico, manifestam-se desde a infância, mesmo que sejam reconhecidos somente mais tarde, são persistentes, geram algum grau de limitação seja na capacidade de aprendizagem, na comunicação, ou na interação social, o que produz reflexos na vida escolar, laboral ou outras áreas da vida. Os principais transtornos do desenvolvimento neural são o transtorno do espectro autista (autismo), a deficiência intelectual (retardo mental ou deficiência mental), o transtorno do déficit de atenção e hiperatividade (TDAH), a epilepsia dos transtornos do desenvolvimento, a dislexia do desenvolvimento, a discalculia do desenvolvimento, a gagueira do desenvolvimento e a paralisia cerebral. Os transtornos do desenvolvimento neural podem ter diversas causas, genéticas e não genéticas (ambientais), e muitas vezes ambas contribuem para a ocorrência do transtorno. O objetivo deste trabalho é compreender os mecanismos envolvidos na origem dos transtornos de desenvolvimento neural durante a formação cerebral a partir de trabalhos da base de dados do índice Medline. Neurodevelopmental disorders are a very diverse group of clinically identifiable disorders that result from derangement of neural development, they are persistent and manifest from childhood, even if they are only recognized later, and generate some degree of limitation in the learning capacity, communication, or social interaction, which produces reflexes in school, work or other areas of life. The main neurodevelopmental disorders are autism spectrum disorder (autism), intellectual disability (mental retardation or mental disability), attention deficit hyperactivity disorder (ADHD), developmental epilepsy, developmental dyslexia, developmental dyscalculia, developmental stuttering and cerebral palsy. Neurodevelopmental disorders may have several causes, genetic and non-genetic (environmental), and often both act simultaneously. The aim of this work is to understand the mechanisms involved in the origin of neural development disorders during brain formation based on words from the Medline index database.

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11

Larson, Charles R. "2008 Zemlin Award in Speech Sciences Memorial Lecture: The Role of Auditory Feedback for the Control of Voice Fundamental Frequency and Amplitude." Perspectives on Speech Science and Orofacial Disorders 19, no. 1 (July 2009): 6–17. http://dx.doi.org/10.1044/ssod19.1.6.

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Abstract Previous research has failed to identify precise neural mechanisms involved in auditory feedback regulation of vocalization. The goal of this research project was to improve our understanding of neural mechanisms controlling the voice. Participants were instructed to sustain a vowel or repeat phrases during which perturbations in voice pitch or loudness feedback were presented. Voice signal averaging, neuroimaging, laryngeal electromyography, and cortical event-related potential techniques were used to measure vocal and neural responses to perturbed feedback. Pitch- and loudness-shifted voice feedback triggers small automatic corrective responses in voice fundamental frequency and amplitude during vowel or speech production. Larger responses during speech suggest task modulation of these responses. Larger responses were also recorded in individuals with Parkinson's disease and children with autism than in normal controls. Neural recording techniques revealed cortical activation during these responses. Cortical mechanisms are involved in generating corrective vocal responses to perturbations in voice auditory feedback. This system helps control the voice during speech and dynamically adjusts responses to meet vocal goals. Abnormally large responses in individuals with Parkinson's disease and autism suggest that the audio-vocal mechanisms just described may be involved in the speech and vocalizations of these individuals as well.

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12

Caron, M. J. "Cognitive mechanisms, specificity and neural underpinnings of visuospatial peaks in autism." Brain 129, no. 7 (July 1, 2006): 1789–802. http://dx.doi.org/10.1093/brain/awl072.

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13

Guerra, Daniel J. "The Molecular Genetics of Autism Spectrum Disorders: Genomic Mechanisms, Neuroimmunopathology, and Clinical Implications." Autism Research and Treatment 2011 (2011): 1–16. http://dx.doi.org/10.1155/2011/398636.

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Autism spectrum disorders (ASDs) have become increasingly common in recent years. The discovery of single-nucleotide polymorphisms and accompanying copy number variations within the genome has increased our understanding of the architecture of the disease. These genetic and genomic alterations coupled with epigenetic phenomena have pointed to a neuroimmunopathological mechanism for ASD. Model animal studies, developmental biology, and affective neuroscience laid a foundation for dissecting the neural pathways impacted by these disease-generating mechanisms. The goal of current autism research is directed toward a systems biological approach to find the most basic genetic and environmental causes to this severe developmental disease. It is hoped that future genomic and neuroimmunological research will be directed toward finding the road toward prevention, treatment, and cure of ASD.

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Rosenblau, Gabriela, Dorit Kliemann, Benjamin Lemme, Henrik Walter, Hauke R. Heekeren, and Isabel Dziobek. "The role of the amygdala in naturalistic mentalising in typical development and in autism spectrum disorder." British Journal of Psychiatry 208, no. 6 (June 2016): 556–64. http://dx.doi.org/10.1192/bjp.bp.114.159269.

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BackgroundThe substantial discrepancy between mentalising in experimental settings v. real-life social interactions hinders the understanding of the neural basis of real-life social cognition and of social impairments in psychiatric disorders.AimsTo determine the neural mechanisms underlying naturalistic mentalising in individuals with and without autism spectrum disorder.MethodWe investigated mentalising with a new video-based functional magnetic resonance imaging task in 20 individuals with autism spectrum disorder and 22 matched healthy controls.ResultsNaturalistic mentalising implicated regions of the traditional mentalising network (medial prefrontal cortex, temporoparietal junction), and additionally the insula and amygdala. Moreover, amygdala activity predicted implicit mentalising performance on an independent behavioural task. Compared with controls, the autism spectrum disorder group did not show differences in neural activity within classical mentalising regions. They did, however, show reduced amygdala activity and a reduced correlation between amygdala activity and mentalising accuracy on the behavioural task, compared with controls.ConclusionsThese findings highlight the crucial role of the amygdala in making accurate implicit mental state inferences in typical development and in the social cognitive impairments of individuals with autism spectrum disorder.

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MENG, Jing, and Lin SHEN. "Empathy in individuals with autism spectrum disorder: Symptoms, theories and neural mechanisms." Advances in Psychological Science 25, no. 1 (2017): 59. http://dx.doi.org/10.3724/sp.j.1042.2017.00059.

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Takano, Tomoyuki. "Role of Microglia in Autism: Recent Advances." Developmental Neuroscience 37, no. 3 (2015): 195–202. http://dx.doi.org/10.1159/000398791.

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The neurobiological basis for autism remains poorly understood. However, the neuroinflammation processes play an important role in the induction of autistic behavioral changes. Microglial cells can exhibit widely differing functions during brain development, including synaptogenesis and stem cell proliferation, in addition to playing a role in the innate immunity. Mounting evidence indicates that microglial activation or dysfunction can profoundly affect neural development, resulting in neurodevelopmental disorders, including autism. These mechanisms in autism have been investigated using neuropathological studies of human autopsy brains, a large number of murine experimental models and in vivo neuroimaging studies of the human brain. The purpose of this review is to discuss microglial activation or dysfunction and to highlight the detrimental role that microglia play in the development of autism. The recent advances presented in this review support that further elucidation of the mechanisms and kinetics of microglial responses will help to establish a window for therapeutic intervention in individuals with autism.

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Iosifyan, M., E. A. Mershina, D. A. Bazhenova, V. E. Sinitsyn, O. M. Larina, and E. V. Pechenkova. "Neural Mechanisms of Theory of Mind in Autism and Schizophrenia: A Review of fMRI Studies." Клиническая и специальная психология 9, no. 1 (2020): 17–46. http://dx.doi.org/10.17759/cpse.2020090102.

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Theory of mind is a cognitive ability, which enables to understand intentions, emotions and beliefs of another person. Because of theory of mind, people are able to interpret behavior of others and adapt to it. Numerous psychiatric impairments are associated with damaged theory of mind and communication with others. The present review analyses the impairments of theory of mind as laying on a continuum from hypermentalization (over-attribution of intentions to others) to hypomentalization (under-attribution of intentions to others) in autism spectrum disorders and schizophrenia. FMRI paradigm of different subprocesses of theory of mind is described (perceptual mind-reading, cognitive theory of mind, “hot” theory of mind and implicit theory of mind). Neural mechanisms of these subprocesses and their impairments in autism spectrum disorder and schizophrenia analyzed.

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Lakshmi Praveena, T., and N. V. Muthu Lakshmi. "Prediction of Autism Spectrum Disorder Using Supervised Machine Learning Algorithms." Asian Journal of Computer Science and Technology 8, no. 3 (November 15, 2019): 15–18. http://dx.doi.org/10.51983/ajcst-2019.8.3.2734.

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Autism appears to be a neuro developmental disorder that is visible in the early years. It is a wide-spectrum disorder that indicates that the severity and symptoms can vary from person to person. The Centre for Disease Control found that one in 68 was diagnosed with autism spectrum disorder with increasing numbers in every year. Detection of autism in adults is a cumbersome procedure because in adults, many symptoms can blend with some other mental health, motor impairment disorders so misinterpretation of actual diseases can in turn lead to a terrible life without proper diagnosis and effective treatment mechanisms. Machine learning is a powerful computer tool that supports different application domains Learning complex relationships or patterns from large datasets to draw accurate conclusions. Disease assessment can be done with predictive health data analysis and more appropriate treatment mechanisms that are now a hot area of research. Supervised learning is an important step of Machine learning which uses a rule-based approach by examining empirical data sets to build accurate predictive models. In this paper, decision tree, random forest, SVM, neural networks algorithms are applied on autism spectrum data which have been collected from UCI repository. The results of decision tree, random forest, SVM, neural networks algorithms on autism dataset are presented in this paper in an efficient manner. Analysis performed over these accurate results which will be useful to make right decisions in predicting autism spectrum disorder (ASD) at early stages. Thus, early autism intervention using machine learning techniques opens up a new way for autistic individuals to develop the potential to lead a better life by improving their behavioural and emotional skills.

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Wang, Ling, Binquan Wang, Chunyan Wu, Jie Wang, and Mingkuan Sun. "Autism Spectrum Disorder: Neurodevelopmental Risk Factors, Biological Mechanism, and Precision Therapy." International Journal of Molecular Sciences 24, no. 3 (January 17, 2023): 1819. http://dx.doi.org/10.3390/ijms24031819.

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Autism spectrum disorder (ASD) is a heterogeneous, behaviorally defined neurodevelopmental disorder. Over the past two decades, the prevalence of autism spectrum disorders has progressively increased, however, no clear diagnostic markers and specifically targeted medications for autism have emerged. As a result, neurobehavioral abnormalities, neurobiological alterations in ASD, and the development of novel ASD pharmacological therapy necessitate multidisciplinary collaboration. In this review, we discuss the development of multiple animal models of ASD to contribute to the disease mechanisms of ASD, as well as new studies from multiple disciplines to assess the behavioral pathology of ASD. In addition, we summarize and highlight the mechanistic advances regarding gene transcription, RNA and non-coding RNA translation, abnormal synaptic signaling pathways, epigenetic post-translational modifications, brain-gut axis, immune inflammation and neural loop abnormalities in autism to provide a theoretical basis for the next step of precision therapy. Furthermore, we review existing autism therapy tactics and limits and present challenges and opportunities for translating multidisciplinary knowledge of ASD into clinical practice.

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WANG, Lin, Zhidan WANG, and Hongjing WANG. "The neural mechanisms of developmental motor disorders in children with autism spectrum disorder." Advances in Psychological Science 29, no. 7 (2021): 1239. http://dx.doi.org/10.3724/sp.j.1042.2021.01239.

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SUN, Yan, Lin FANG, Tingyu WANG, and Li CUI. "The influence factors and neural mechanisms of inhibitory control in autism spectrum disorders." Advances in Psychological Science 26, no. 8 (2018): 1450. http://dx.doi.org/10.3724/sp.j.1042.2018.01450.

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Greimel, Ellen, Martin Schulte-Rüther, Tilo Kircher, Inge Kamp-Becker, Helmut Remschmidt, Gereon R. Fink, Beate Herpertz-Dahlmann, and Kerstin Konrad. "Neural mechanisms of empathy in adolescents with autism spectrum disorder and their fathers." NeuroImage 49, no. 1 (January 2010): 1055–65. http://dx.doi.org/10.1016/j.neuroimage.2009.07.057.

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Barman, Adriana, Sylvia Richter, Joram Soch, Anna Deibele, Anni Richter, Anne Assmann, Torsten Wüstenberg, Henrik Walter, Constanze I. Seidenbecher, and Björn H. Schott. "Gender-specific modulation of neural mechanisms underlying social reward processing by Autism Quotient." Social Cognitive and Affective Neuroscience 10, no. 11 (May 4, 2015): 1537–47. http://dx.doi.org/10.1093/scan/nsv044.

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Wenderski, Wendy, Lu Wang, Andrey Krokhotin, Jessica J. Walsh, Hongjie Li, Hirotaka Shoji, Shereen Ghosh, et al. "Loss of the neural-specific BAF subunit ACTL6B relieves repression of early response genes and causes recessive autism." Proceedings of the National Academy of Sciences 117, no. 18 (April 20, 2020): 10055–66. http://dx.doi.org/10.1073/pnas.1908238117.

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Synaptic activity in neurons leads to the rapid activation of genes involved in mammalian behavior. ATP-dependent chromatin remodelers such as the BAF complex contribute to these responses and are generally thought to activate transcription. However, the mechanisms keeping such “early activation” genes silent have been a mystery. In the course of investigating Mendelian recessive autism, we identified six families with segregating loss-of-function mutations in the neuronal BAF (nBAF) subunit ACTL6B (originally named BAF53b). Accordingly, ACTL6B was the most significantly mutated gene in the Simons Recessive Autism Cohort. At least 14 subunits of the nBAF complex are mutated in autism, collectively making it a major contributor to autism spectrum disorder (ASD). Patient mutations destabilized ACTL6B protein in neurons and rerouted dendrites to the wrong glomerulus in the fly olfactory system. Humans and mice lacking ACTL6B showed corpus callosum hypoplasia, indicating a conserved role for ACTL6B in facilitating neural connectivity. Actl6b knockout mice on two genetic backgrounds exhibited ASD-related behaviors, including social and memory impairments, repetitive behaviors, and hyperactivity. Surprisingly, mutation of Actl6b relieved repression of early response genes including AP1 transcription factors (Fos, Fosl2, Fosb, and Junb), increased chromatin accessibility at AP1 binding sites, and transcriptional changes in late response genes associated with early response transcription factor activity. ACTL6B loss is thus an important cause of recessive ASD, with impaired neuron-specific chromatin repression indicated as a potential mechanism.

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Benvenuto, A., B. Manzi, R. Alessandrelli, C. Galasso, and P. Curatolo. "Recent Advances in the Pathogenesis of Syndromic Autisms." International Journal of Pediatrics 2009 (2009): 1–9. http://dx.doi.org/10.1155/2009/198736.

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Background. Current advances in genetic technology continue to expand the list of medical conditions associated with autism. Clinicians have to identify specific autistic-related syndromes, and to provide tailored counseling. The aim of this study is to elucidate recent advances in autism research that offer important clues into pathogenetic mechanisms of syndromic autism and relevant implications for clinical practice.Data Sources. The PubMed database was searched with the keywords “autism” and “chromosomal abnormalities,” “metabolic diseases,” “susceptibility loci.”Results. Defined mutations, genetic syndromes, and metabolic diseases account for up to 20% of autistic patients. Metabolic and mitochondrial defects may have toxic effects on the brain cells, causing neuronal loss and altered modulation of neurotransmission systems. Alterations of the neocortical excitatory/inhibitory balance and perturbations of interneurons' development represent the most probable pathogenetic mechanisms underlying the autistic phenotype in Fragile X-Syndrome and Tuberous Sclerosis Complex. Chromosomal abnormalities and potential candidate genes are strongly implicated in the disruption of neural connections, brain growth, and synaptic/dendritic morphology.Conclusion. Metabolic testing may be appropriate if specific symptoms are present. High-resolution chromosome analysis may be recommended if a specific diagnosis is suspected because of obvious dysmorphisms. Identifying cryptic chromosomal abnormalities by whole genome microarray analysis can increase the understanding of the neurobiological pathways to autism.

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Tager-Flusberg, Helen. "Risk Factors Associated With Language in Autism Spectrum Disorder: Clues to Underlying Mechanisms." Journal of Speech, Language, and Hearing Research 59, no. 1 (February 2016): 143–54. http://dx.doi.org/10.1044/2015_jslhr-l-15-0146.

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Purpose Identifying risk factors associated with neurodevelopmental disorders is an important line of research, as it will lead to earlier identification of children who could benefit from interventions that support optimal developmental outcomes. The primary goal of this review was to summarize research on risk factors associated with autism spectrum disorder (ASD). Method The review focused on studies of infants who have older siblings with ASD, with particular emphasis on risk factors associated with language impairment that affects the majority of children with ASD. Findings from this body of work were compared to the literature on specific language impairment. Results A wide range of risk factors has been found for ASD, including demographic (e.g., male, family history), behavioral (e.g., gesture, motor) and neural risk markers (e.g., atypical lateralization for speech and reduced functional connectivity). Environmental factors, such as caregiver interaction, have not been found to predict language outcomes. Many of the risk markers for ASD are also found in studies of risk for specific language impairment, including demographic, behavioral, and neural factors. Conclusions There are significant gaps in the literature and limitations in the current research that preclude direct cross-syndrome comparisons. Future research directions are outlined that could address these limitations.

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Beker, Shlomit, John J. Foxe, and Sophie Molholm. "Oscillatory entrainment mechanisms and anticipatory predictive processes in children with autism spectrum disorder." Journal of Neurophysiology 126, no. 5 (November 1, 2021): 1783–98. http://dx.doi.org/10.1152/jn.00329.2021.

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We examined behavioral and EEG indices of predictive processing in children with ASD to rhythmically predictable stimuli. Although behavioral measures of predictive processing and evoked neural responses were intact in the ASD group, neurophysiological measures of preparatory activity and entrainment were impaired. When sensory events are presented in a predictable temporal pattern, performance and neuronal responses in ASD may be governed more by the occurrence of the events themselves and less by their anticipated timing.

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Wood, Emily T., Jillian Melbourne, Shulamite Green, Susan Y. Bookheimer, and Mirella Dapretto. "6.35 Behavioral and Neural Mechanisms of Trauma Symptomatology in Youth With Autism Spectrum Disorder." Journal of the American Academy of Child & Adolescent Psychiatry 60, no. 10 (October 2021): S169—S170. http://dx.doi.org/10.1016/j.jaac.2021.09.399.

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Greimel, Ellen, Barbara Nehrkorn, Gereon R. Fink, Juraj Kukolja, Gregor Kohls, Kristin Müller, Martina Piefke, et al. "Neural mechanisms of encoding social and non-social context information in autism spectrum disorder." Neuropsychologia 50, no. 14 (December 2012): 3440–49. http://dx.doi.org/10.1016/j.neuropsychologia.2012.09.029.

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BROCK, JON, CAROLINE C. BROWN, JILL BOUCHER, and GINA RIPPON. "The temporal binding deficit hypothesis of autism." Development and Psychopathology 14, no. 2 (May 15, 2002): 209–24. http://dx.doi.org/10.1017/s0954579402002018.

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Frith has argued that people with autism show “weak central coherence,” an unusual bias toward piecemeal rather than configurational processing and a reduction in the normal tendency to process information in context. However, the precise cognitive and neurological mechanisms underlying weak central coherence are still unknown. We propose the hypothesis that the features of autism associated with weak central coherence result from a reduction in the integration of specialized local neural networks in the brain caused by a deficit in temporal binding. The visuoperceptual anomalies associated with weak central coherence may be attributed to a reduction in synchronization of high-frequency gamma activity between local networks processing local features. The failure to utilize context in language processing in autism can be explained in similar terms. Temporal binding deficits could also contribute to executive dysfunction in autism and to some of the deficits in socialization and communication.

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Stroganova, T. A., E. V. Orekhova, and I. A. Galuta. "Neural basis of attention orienting abnormalities in children with autism." Experimental Psychology (Russia) 8, no. 3 (2015): 7–23. http://dx.doi.org/10.17759/exppsy.2015080302.

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Detection of new events occurring outside the focus of attention is fundamental to adaptive functioning and is most critical when attention is focused elsewhere. The unattended novel sensory events may demand further analysis according to their task relevance and may appear important for survival. Behavioral and physiological findings reviewed in this article imply that brains of many people with autism spectrum disorders (ASD) are, to a certain extent, impenetrable to such unattended but potentially salient changes in the immediate sensory environment. Here we reviewed neurophysiological studies investigating neural processing of salient (rare, novel or deviant) auditory stimuli in ASD. We put forward a hypothesis that atypical processing of deviance and novelty in a proportion of individuals with ASD may be grounded in the failure of nicotinic cholinergic arousal pathways to engage cortical mechanisms involved in detection of changes in the environment and appraisal of their novelty, if these changes occur beyond the currently attended sensory stream. Further studies linking neurophysiological findings with attention behavior and those searching for their neurochemical and genetic bases will help to understand causes of attention problems and sensory modulation difficulties in children with ASD and may prove helpful to direct early intervention

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Gonzalez-Gadea, Maria Luz, Srivas Chennu, Tristan A. Bekinschtein, Alexia Rattazzi, Ana Beraudi, Paula Tripicchio, Beatriz Moyano, et al. "Predictive coding in autism spectrum disorder and attention deficit hyperactivity disorder." Journal of Neurophysiology 114, no. 5 (November 2015): 2625–36. http://dx.doi.org/10.1152/jn.00543.2015.

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Predictive coding has been proposed as a framework to understand neural processes in neuropsychiatric disorders. We used this approach to describe mechanisms responsible for attentional abnormalities in autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD). We monitored brain dynamics of 59 children (8–15 yr old) who had ASD or ADHD or who were control participants via high-density electroencephalography. We performed analysis at the scalp and source-space levels while participants listened to standard and deviant tone sequences. Through task instructions, we manipulated top-down expectation by presenting expected and unexpected deviant sequences. Children with ASD showed reduced superior frontal cortex (FC) responses to unexpected events but increased dorsolateral prefrontal cortex (PFC) activation to expected events. In contrast, children with ADHD exhibited reduced cortical responses in superior FC to expected events but strong PFC activation to unexpected events. Moreover, neural abnormalities were associated with specific control mechanisms, namely, inhibitory control in ASD and set-shifting in ADHD. Based on the predictive coding account, top-down expectation abnormalities could be attributed to a disproportionate reliance (precision) allocated to prior beliefs in ASD and to sensory input in ADHD.

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Kim, So Hyun, George Buzzell, Susan Faja, Yeo Bi Choi, Hannah R. Thomas, Natalie Hiromi Brito, Lauren C. Shuffrey, et al. "Neural dynamics of executive function in cognitively able kindergarteners with autism spectrum disorders as predictors of concurrent academic achievement." Autism 24, no. 3 (December 3, 2019): 780–94. http://dx.doi.org/10.1177/1362361319874920.

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Although electrophysiological (electroencephalography) measures of executive functions (e.g. error monitoring) have been used to predict academic achievement in typically developing children, work investigating a link between error monitoring and academic skills in children with autism spectrum disorder is limited. In this study, we employed traditional electrophysiological and advanced time–frequency methods, combined with principal component analyses, to extract neural activity related to error monitoring and tested their relations to academic achievement in cognitively able kindergarteners with autism spectrum disorder. In total, 35 cognitively able kindergarteners with autism spectrum disorder completed academic assessments and the child-friendly “Zoo Game” Go/No-go task at school entry. The Go/No-go task successfully elicited an error-related negativity and error positivity in children with autism spectrum disorder as young as 5 years at fronto-central and posterior electrode sites, respectively. We also observed increased response-related theta power during errors relative to correct trials at fronto-central sites. Both larger error positivity and theta power significantly predicted concurrent academic achievement after controlling for behavioral performance on the Zoo Game and intelligence quotient. These results suggest that the use of time–frequency electroencephalography analyses, combined with traditional event-related potential measures, may provide new opportunities to investigate neurobiological mechanisms of executive function and academic achievement in young children with autism spectrum disorder.

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Blatt, Gene J. "The Neuropathology of Autism." Scientifica 2012 (2012): 1–16. http://dx.doi.org/10.6064/2012/703675.

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Autism is a behaviorally defined neurodevelopmental disorder that affects over 1% of new births in the United States and about 2% of boys. The etiologies are unknown and they are genetically complex. There may be epigenetic effects, environmental influences, and other factors that contribute to the mechanisms and affected neural pathway(s). The underlying neuropathology of the disorder has been evolving in the literature to include specific brain areas in the cerebellum, limbic system, and cortex. Part(s) of structures appear to be affected most rather than the entire structure, for example, select nuclei of the amygdala, the fusiform face area, and so forth. Altered cortical organization characterized by more frequent and narrower minicolumns and early overgrowth of the frontal portion of the brain, affects connectivity. Abnormalities include cytoarchitectonic laminar differences, excess white matter neurons, decreased numbers of GABAergic cerebellar Purkinje cells, and other events that can be traced developmentally and cause anomalies in circuitry. Problems with neurotransmission are evident by recent receptor and binding site studies especially in the inhibitory GABA system likely contributing to an imbalance of excitatory/inhibitory transmission. As postmortem findings are related to core behavior symptoms, and technology improves, researchers are gaining a much better perspective of contributing factors to the disorder.

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CHEN, Xiaowen, Wenshu CAI, Tong XIE, and Shimin FU. "The characteristics and neural mechanisms of visual orienting and visual search in autism spectrum disorders." Advances in Psychological Science 28, no. 1 (2020): 98. http://dx.doi.org/10.3724/sp.j.1042.2020.00098.

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Thomas, Michael S. C., Victoria C. P. Knowland, and Annette Karmiloff-Smith. "Mechanisms of developmental regression in autism and the broader phenotype: A neural network modeling approach." Psychological Review 118, no. 4 (2011): 637–54. http://dx.doi.org/10.1037/a0025234.

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Sullivan, Katherine, Wendy L. Stone, and Geraldine Dawson. "Potential neural mechanisms underlying the effectiveness of early intervention for children with autism spectrum disorder." Research in Developmental Disabilities 35, no. 11 (November 2014): 2921–32. http://dx.doi.org/10.1016/j.ridd.2014.07.027.

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Dubischar-Krivec, Anna Milena, Sven Bölte, Christoph Braun, Fritz Poustka, Niels Birbaumer, and Nicola Neumann. "Neural mechanisms of savant calendar calculating in autism: An MEG-study of few single cases." Brain and Cognition 90 (October 2014): 157–64. http://dx.doi.org/10.1016/j.bandc.2014.07.003.

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Kinard, Jessica Lynn, Maya Gelman Mosner, Rachel Kirsten Greene, Merideth Addicott, Joshua Bizzell, Chris Petty, Paul Cernasov, et al. "Neural Mechanisms of Social and Nonsocial Reward Prediction Errors in Adolescents with Autism Spectrum Disorder." Autism Research 13, no. 5 (February 11, 2020): 715–28. http://dx.doi.org/10.1002/aur.2273.

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Jerger, Kristin K., Laura Lundegard, Aaron Piepmeier, Keturah Faurot, Amanda Ruffino, Margaret A. Jerger, and Aysenil Belger. "Neural Mechanisms of Qigong Sensory Training Massage for Children With Autism Spectrum Disorder: A Feasibility Study." Global Advances in Health and Medicine 7 (January 2018): 216495611876900. http://dx.doi.org/10.1177/2164956118769006.

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Objectives Despite the enormous prevalence of autism spectrum disorder (ASD), its global impact has yet to be realized. Millions of families worldwide need effective treatments to help them get through everyday challenges like eating, sleeping, digestion, and social interaction. Qigong Sensory Training (QST) is a nonverbal, parent-delivered intervention recently shown to be effective at reducing these everyday challenges in children with ASD. This study tested the feasibility of a protocol for investigating QST’s neural mechanism. Methods During a single visit, 20 children, 4- to 7-year-old, with ASD viewed images of emotional faces before and after receiving QST or watching a video (controls). Heart rate variability was recorded throughout the visit, and power in the high frequency band (0.15–0.4 Hz) was calculated to estimate parasympathetic tone in 5-s nonoverlapping windows. Cerebral oximetry of prefrontal cortex was recorded during rest and while viewing emotional faces. Results 95% completion rate and 7.6% missing data met a priori standards confirming protocol feasibility for future studies. Preliminary data suggest: (1) during the intervention, parasympathetic tone increased more in children receiving massage (M = 2.9, SD = 0.3) versus controls (M = 2.5, SD = 0.5); (2) while viewing emotional faces post-intervention, parasympathetic tone was more affected (reduced) in the massage group ( p = 0.036); and (3) prefrontal cortex response to emotional faces was greater after massage compared to controls. These results did not reach statistical significance in this small study powered to test feasibility. Discussion/Conclusion This study demonstrates solid protocol feasibility. If replicated in a larger sample, these findings would provide important clues to the neural mechanism of action underlying QST’s efficacy for improving sensory, social, and communication difficulties in children with autism.

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Siniscalco, Dario, Anna Sapone, Alessandra Cirillo, Catia Giordano, Sabatino Maione, and Nicola Antonucci. "Autism Spectrum Disorders: Is Mesenchymal Stem Cell Personalized Therapy the Future?" Journal of Biomedicine and Biotechnology 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/480289.

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Autism and autism spectrum disorders (ASDs) are heterogeneous neurodevelopmental disorders. They are enigmatic conditions that have their origins in the interaction of genes and environmental factors. ASDs are characterized by dysfunctions in social interaction and communication skills, in addition to repetitive and stereotypic verbal and nonverbal behaviours. Immune dysfunction has been confirmed with autistic children. There are no defined mechanisms of pathogenesis or curative therapy presently available. Indeed, ASDs are still untreatable. Available treatments for autism can be divided into behavioural, nutritional, and medical approaches, although no defined standard approach exists. Nowadays, stem cell therapy represents the great promise for the future of molecular medicine. Among the stem cell population, mesenchymal stem cells (MSCs) show probably best potential good results in medical research. Due to the particular immune and neural dysregulation observed in ASDs, mesenchymal stem cell transplantation could offer a unique tool to provide better resolution for this disease.

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Blair, R. J. R. "Facial expressions, their communicatory functions and neuro–cognitive substrates." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 358, no. 1431 (February 5, 2003): 561–72. http://dx.doi.org/10.1098/rstb.2002.1220.

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Human emotional expressions serve a crucial communicatory role allowing the rapid transmission of valence information from one individual to another. This paper will review the literature on the neural mechanisms necessary for this communication: both the mechanisms involved in the production of emotional expressions and those involved in the interpretation of the emotional expressions of others. Finally, reference to the neuro–psychiatric disorders of autism, psychopathy and acquired sociopathy will be made. In these conditions, the appropriate processing of emotional expressions is impaired. In autism, it is argued that the basic response to emotional expressions remains intact but that there is impaired ability to represent the referent of the individual displaying the emotion. In psychopathy, the response to fearful and sad expressions is attenuated and this interferes with socialization resulting in an individual who fails to learn to avoid actions that result in harm to others. In acquired sociopathy, the response to angry expressions in particular is attenuated resulting in reduced regulation of social behaviour.

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Nguyen, Anna O., Devin K. Binder, Iryna M. Ethell, and Khaleel A. Razak. "Abnormal development of auditory responses in the inferior colliculus of a mouse model of Fragile X Syndrome." Journal of Neurophysiology 123, no. 6 (June 1, 2020): 2101–21. http://dx.doi.org/10.1152/jn.00706.2019.

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Autism spectrum disorders (ASD) are commonly associated with sensory sensitivity issues, but the underlying mechanisms are unclear. This study presents novel evidence for neural correlates of auditory hypersensitivity in the developing inferior colliculus (IC) in the Fmr1 knockout (KO) mouse, a mouse model of Fragile X Syndrome (FXS), a leading genetic cause of ASD. Responses begin to show genotype differences between postnatal days 14 and 21, suggesting an early developmental treatment window.

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Lucker, Jay R., and Alex Doman. "Neural Mechanisms Involved in Hypersensitive Hearing: Helping Children with ASD Who Are Overly Sensitive to Sounds." Autism Research and Treatment 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/369035.

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Professionals working with children diagnosed with autism spectrum disorder (ASD) may find that these children are overly sensitive to sounds. These professionals are often concerned as to why children may have auditory hypersensitivities. This review article discusses the neural mechanisms identified underlying hypersensitive hearing in people. The authors focus on brain research to support the idea of the nonclassical auditory pathways being involved in connecting the auditory system with the emotional system of the brain. The authors also discuss brain mechanisms felt to be involved in auditory hypersensitivity. The authors conclude with a discussion of some treatments for hypersensitive hearing. These treatments include desensitization training and the use of listening therapies such as The Listening Program.

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Hayot, Gaëlle, Mathieu Massonot, Céline Keime, Elodie Faure, and Christelle Golzio. "Loss of autism-candidate CHD8 perturbs neural crest development and intestinal homeostatic balance." Life Science Alliance 6, no. 1 (November 14, 2022): e202201456. http://dx.doi.org/10.26508/lsa.202201456.

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Individuals with mutations inCHD8present with gastrointestinal complaints, yet the underlying mechanisms are understudied. Here, using a stable constitutivechd8mutant zebrafish model, we found that the loss ofchd8leads to a reduced number of vagal neural crest cells (NCCs), enteric neural and glial progenitors, emigrating from the neural tube, and that their early migration capability was altered. At later stages, although the intestinal colonization by NCCs was complete, we found the decreased numbers of both serotonin-producing enterochromaffin cells and NCC-derived serotonergic neurons, suggesting an intestinal hyposerotonemia in the absence ofchd8. Furthermore, transcriptomic analyses revealed an altered expression of key receptors and enzymes in serotonin and acetylcholine signaling pathways. The tissue examination ofchd8mutants revealed a thinner intestinal epithelium accompanied by an accumulation of neutrophils and the decreased numbers of goblet cells and eosinophils. Last, single-cell sequencing of whole intestines showed a global disruption of the immune balance with a perturbed expression of inflammatory interleukins and changes in immune cell clusters. Our findings propose a causal developmental link betweenchd8, NCC development, intestinal homeostasis, and autism-associated gastrointestinal complaints.

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White, Susan W., Carla A. Mazefsky, Gabriel S. Dichter, Pearl H. Chiu, John A. Richey, and Thomas H. Ollendick. "Social‐cognitive, physiological, and neural mechanisms underlying emotion regulation impairments: understanding anxiety in autism spectrum disorder." International Journal of Developmental Neuroscience 39, no. 1 (June 18, 2014): 22–36. http://dx.doi.org/10.1016/j.ijdevneu.2014.05.012.

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Eigsti, Inge-Marie, and Jillian M. Schuh. "NEUROBIOLOGICAL UNDERPINNINGS OF LANGUAGE IN AUTISM SPECTRUM DISORDERS." Annual Review of Applied Linguistics 28 (March 2008): 128–49. http://dx.doi.org/10.1017/s0267190508080021.

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As a neurodevelopmental disorder, autism is characterized by impairments and differences at the levels of both brain and behavior. Communicative impairments in autism are a core feature of the disorder, and a rapidly expanding literature is exploring language in autism using the tools of cognitive neuroscience, particularly electroencephalography and brain imaging. Recent research indicates consistent differences in the degree to which language-specific processes are lateralized in the brain, and it also suggests that language impairments are linked to differences in brain structure that may lead to inefficient coordination of activity between different neural assemblies to achieve a complex cognitive task, defined as functional connectivity. We review findings from current work and suggest that neurobiological data are critical in our ability to understand the mechanisms underlying behavioral differences in communicative skills. Going beyond simple dichotomies between delayed versus deviant development, we can use such data to ask whether behavior reflects processes that are merely inefficient or, instead, whether impairments at the behavioral level reflect fundamental differences in brain organization and the networks involved in various tasks.

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Li, Dan, Joshua Xu, and Mary Qu Yang. "Gene Regulation Analysis Reveals Perturbations of Autism Spectrum Disorder during Neural System Development." Genes 12, no. 12 (November 27, 2021): 1901. http://dx.doi.org/10.3390/genes12121901.

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Autism spectrum disorder (ASD) is a neurodevelopmental disorder that impedes patients’ cognition, social, speech and communication skills. ASD is highly heterogeneous with a variety of etiologies and clinical manifestations. The prevalence rate of ASD increased steadily in recent years. Presently, molecular mechanisms underlying ASD occurrence and development remain to be elucidated. Here, we integrated multi-layer genomics data to investigate the transcriptome and pathway dysregulations in ASD development. The RNA sequencing (RNA-seq) expression profiles of induced pluripotent stem cells (iPSCs), neural progenitor cells (NPCs) and neuron cells from ASD and normal samples were compared in our study. We found that substantially more genes were differentially expressed in the NPCs than the iPSCs. Consistently, gene set variation analysis revealed that the activity of the known ASD pathways in NPCs and neural cells were significantly different from the iPSCs, suggesting that ASD occurred at the early stage of neural system development. We further constructed comprehensive brain- and neural-specific regulatory networks by incorporating transcription factor (TF) and gene interactions with long 5 non-coding RNA(lncRNA) and protein interactions. We then overlaid the transcriptomes of different cell types on the regulatory networks to infer the regulatory cascades. The variations of the regulatory cascades between ASD and normal samples uncovered a set of novel disease-associated genes and gene interactions, particularly highlighting the functional roles of ELF3 and the interaction between STAT1 and lncRNA ELF3-AS 1 in the disease development. These new findings extend our understanding of ASD and offer putative new therapeutic targets for further studies.

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Lin, I. Fan, Aya Shirama, Nobumasa Kato, and Makio Kashino. "The singular nature of auditory and visual scene analysis in autism." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1714 (February 19, 2017): 20160115. http://dx.doi.org/10.1098/rstb.2016.0115.

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Individuals with autism spectrum disorder often have difficulty acquiring relevant auditory and visual information in daily environments, despite not being diagnosed as hearing impaired or having low vision. Resent psychophysical and neurophysiological studies have shown that autistic individuals have highly specific individual differences at various levels of information processing, including feature extraction, automatic grouping and top-down modulation in auditory and visual scene analysis. Comparison of the characteristics of scene analysis between auditory and visual modalities reveals some essential commonalities, which could provide clues about the underlying neural mechanisms. Further progress in this line of research may suggest effective methods for diagnosing and supporting autistic individuals. This article is part of the themed issue ‘Auditory and visual scene analysis'.

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Siracusano, Martina, Assia Riccioni, Roberta Abate, Arianna Benvenuto, Paolo Curatolo, and Luigi Mazzone. "Vitamin D Deficiency and Autism Spectrum Disorder." Current Pharmaceutical Design 26, no. 21 (June 24, 2020): 2460–74. http://dx.doi.org/10.2174/1381612826666200415174311.

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: Vitamin D is a neurosteroid hormone crucially involved in neurodevelopment. Neural cell proliferation, neurotransmission, oxidative stress and immune function represent the main mechanisms mediated by vitamin D in the Central Nervous System. Therefore, its deficiency during pregnancy and early childhood may significantly impact on a developing brain, leading to possible adverse neuropsychological outcomes including Autism Spectrum Disorder (ASD). Significant vitamin D deficiency is described within children affected by ASD and in pregnant mothers whose offspring will later develop ASD, suggesting a possible role of the hormone as a contributing risk factor in the etiopathogenesis of ASD. We reviewed the actual literature on the potential contributing role of prenatal and early postnatal vitamin D deficiency in ASD etiopathogenesis, at both genetic and environmental levels, and the possible effect of vitamin D supplementation in autistic children. Conflicting but promising results emerged on the topic. : Further Randomized Controlled Trials studies carried out during pregnancy and early infancy are necessary for better understanding the possible contribution of vitamin D deficiency in the etiopathogenesis of autism and the potential efficacy of the hormone supplementation in the improvement of ASD core symptoms.

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