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Статті в журналах з теми "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.
Повний текст джерелаАнотація:
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.
Повний текст джерелаАнотація:
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.
Повний текст джерелаАнотація:
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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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.
Повний текст джерелаАнотація:
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.
Повний текст джерелаАнотація:
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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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.
Повний текст джерелаАнотація:
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.
Повний текст джерелаАнотація:
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.
Повний текст джерелаАнотація:
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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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.
Повний текст джерелаАнотація:
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.
Дисертації з теми "Neural mechanisms autism"
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Lefevre, Arthur. "Neural mechanisms of oxytocin and serotonin interaction in non-human primates and patients with autism." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE1323/document.
Повний текст джерелаАнотація:
La neurohormone ocytocine (OT) est de plus en plus étudiée pour son potentiel thérapeutique dans les troubles du comportement social, comme l'autisme, qui sont associés à une dérégulation de plusieurs systèmes de neurotransmission, notamment l'OT et la sérotonine (5-HT). Dans ce cadre, une étape importante afin de développer des médicaments basés sur des mécanismes biologiques est de caractériser les interactions entre l'OT et les autres neurotransmetteurs. La littérature sur les rongeurs montre que la relation entre OT et 5-HT est fortement impliquée dans plusieurs aspects du comportement social. Par ailleurs, nous avons récemment montré chez le sujet sain que le fonctionnement du récepteur 5-HT 1A (5-HT1AR) est modifié suite à l'administration d'OT.neuroJ'ai donc réalisé une première expérience chez des patients autistes en utilisant le scanner TEP avec le radiotraceur [18F]MPPF (spécifique du 5-HT1AR). Aucune différence n'est apparue, à l'état basal, entre 18 patients autistes et 24 sujets contrôles. Par ailleurs, l'OT n'a pas modifié le système 5-HT1AR. Enfin, alors qu'une corrélation entre la densité de 5-HT1AR et le volume de matière grise du striatum a été observé dans le groupe contrôle, cette relation était absente dans le groupe de patients. Ces résultats suggèrent une altération subtile du 5-HT1AR, ne pouvant être détectée qu'au niveau fonctionnel.Parce que le scanner TEP ne permet pas de dire si les changements observés sont dus à une libération de sérotonine ou à une modification directe du récepteur, j'ai réalisé une deuxième expérience chez 3 macaques rhésus, avec le [18F]MPPF et le [11C]DASB (marquant le transporteur de la 5-HT). Par rapport au placebo, l'OT injectée dans le ventricule latéral a significativement augmenté la liaison du [18F]MPPF dans l'amygdale et l'insula tandis que la liaison du [11C]DASB diminuait dans ces mêmes régions. Ainsi, nous pouvons dire que l'OT a provoqué la libération de 5-HT ainsi qu'une modification du 5-HT1AR dans ces régions importantes pour les comportements socio-émotionnels. Une étude par autoradiographie a confirmé cette interprétation.Ces expériences montrent qu'il existe une action régulatrice de l'OT sur la 5-HT chez le primate, mais que ce mécanisme est dérégulé chez les patients avec autisme. Cela ouvre donc la voie à l'investigation de traitements combinés exerçant un effet sur ces deux neurotransmetteursThe neurohormone oxytocin (OT) is increasingly studied for its therapeutic potential in social disorders, like autism, which are associated with the deregulation of several neurotransmission systems, including OT and serotonin (5-HT). Hence investigating OT’s interactions with other neurotransmitters is a relevant step towards mechanism-based treatments. Studies in rodents demonstrated that the interaction between OT and 5-HT, is critical for several aspects of social behaviour. Moreover, using PET-scan in humans we have recently found that 5-HT 1A receptor (5-HT1AR) function is modified after intra-nasal oxytocin intake. Thus I performed a first experiment in which intra-nasal OT was administered to patients with autism undergoing a [18F]MPPF (a 5-HT1AR radiotracer) PET scanner, in order to study their basal serotonergic system and to look if the oxytocin modulates the 5-HT1AR system. I found no differences of baseline 5-HT1AR concentration between 18 autistic subjects and 24 controls. Critically, in patients, OT did not induce changes on the 5-HT1AR system. Moreover, in controls, there was a correlation between 5-HT1AR and grey matter volume in the striatum, that was not observed in patients. These results suggest a subtle disruption of patients’ serotonergic system, that can only be seen at the functional level. Because PET scan does not tell us if the observed modification is due to a change in 5-HT1AR or 5-HT concentration, I performed a second PET scan experiment on 3 macaque monkeys, using [18F]MPPF and [11C]DASB, that marks the serotonin transporter. Compared to placebo, OT injections in the lateral ventricle significantly reduced [11C]DASB binding potential in right amygdala, insula and hippocampus whereas [18F]MPPF binding potential increased in right amygdala and insula. Thus we reproduced results obtained in healthy humans and extended it by suggesting that OT provokes the release of 5-HT in key limbic regions involved in socio-emotional processing. These results were confirmed with autoradiography.Taken together, these experiments indicate that OT modulates 5-HT release in primates, but this mechanism is disrupted in patients with autism. This opens ways to investigate combined OT/5-HT treatments, especially since FDA approved drugs targeting the two systems are already available for use in patients with autism
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Lombardo, Michael. "Cognitive and neural mechanisms underlying self-referential and social cognition in autism and the general population." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608982.
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Coffman, Marika Cerie. "Common and Distinct Neural Mechanisms of Fear Acquisition and Reversal in comorbid Autism with Social Anxiety and Social Anxiety Disorder uncomplicated by Autism." Diss., Virginia Tech, 2019. http://hdl.handle.net/10919/102409.
Повний текст джерелаАнотація:
Social Anxiety (SAD) increases in prevalence as children enter adolescence. Adolescents with Autism Spectrum Disorder (ASD) are diagnosed with comorbid SAD at higher rates than these individuals are diagnosed with other clinical disorders, including depression and other anxiety disorders. However, there is little research on whether the presentation and neural underpinning of comorbid SAD within the context of ASD is the same as SAD alone. Individual and diagnostic differences exist in neural and biological mechanisms of fear conditioning. Characterization of whether neural mechanisms of fear are different within ASD with comorbid SAD and SAD alone may better inform clinical treatments. Accordingly, the present study characterizes neural responses during a fear-inducing experiment, as measured by fMRI. Fifty-seven adolescents participated in this study, with adolescents with ASD and SAD (n=17), SAD alone (n=20), and typically developing adolescents (n=20). All participants completed two fear conditioning and reversal paradigms while completing an fMRI scan. The paradigm consisted of a Social condition and Nonsocial condition. An ANOVA for fear conditioning was conducted. Results revealed significant activation in the Inferior Temporal Gyrus (ITG) during fear conditioning. No between group differences were observed, but within-group differences indicated differential modulation of the ITG in the ASD with SAD group in the Social condition compared to the Nonsocial condition. The SAD group demonstrated differential activation between conditioning stimuli in the Nonsocial condition, but not in the Social condition. Results indicate that adolescents with ASD and SAD may display different neural mechanisms for acquiring fear compared to typically developing peers. Results have potential to inform treatment approaches.Doctor of Philosophy
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Peng, Yun, Zhongming Lu, Guohui Li, Mariel Piechowicz, Miranda Anderson, Yasin Uddin, Jie Wu, and Shengfeng Qiu. "The autism associated MET receptor tyrosine kinase engages early neuronal growth mechanism and controls glutamatergic circuits development in the forebrain." NATURE PUBLISHING GROUP, 2016. http://hdl.handle.net/10150/617181.
Повний текст джерелаАнотація:
The human MET gene imparts a replicated risk for autism spectrum disorder (ASD), and is implicated in
the structural and functional integrity of brain. MET encodes a receptor tyrosine kinase, MET, which
plays a pleiotropic role in embryogenesis and modifies a large number of neurodevelopmental events.
Very little is known, however, on how MET signaling engages distinct cellular events to collectively affect
brain development in ASD-relevant disease domains. Here, we show that MET protein expression is
dynamically regulated and compartmentalized in developing neurons. MET is heavily expressed in
neuronal growth cones at early developmental stages and its activation engages small GTPase Cdc42 to
promote neuronal growth, dendritic arborization, and spine formation. Genetic ablation of MET
signaling in mouse dorsal pallium leads to altered neuronal morphology indicative of early functional
maturation. In contrast, prolonged activation of MET represses the formation and functional
maturation of glutamatergic synapses. Moreover, manipulating MET signaling levels in vivo in the
developing prefrontal projection neurons disrupts the local circuit connectivity made onto these
neurons. Therefore, normal time-delimited MET signaling is critical in regulating the timing of neuronal
growth, glutamatergic synapse maturation and cortical circuit function. Dysregulated MET signaling may
lead to pathological changes in forebrain maturation and connectivity, and thus contribute to the
emergence of neurological symptoms associated with ASD.
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Liao, Chuan-Ching, and 廖專晶. "Different Neural Mechanisms of Semantic Processing Among Youths with Autism Spectrum Disorder, their Unaffected Siblings and Typically Developing Youths." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/6upj59.
Повний текст джерелаАнотація:
碩士國立臺灣大學
心理學研究所
107
Autism spectrum disorder (ASD) is characterized as a highly heritable disorder, and aberrant semantic processing is one of common symptoms in individuals with ASD. Unaffected ASD siblings usually have similar genetic backgrounds and early-life environments with individuals with ASD, with a higher risk of developing the same disorder. However, little is known about genetic contributions to neural mechanisms of semantic processing in unaffected ASD siblings. Therefore, this study aimed to adopt an endophenotype approach to investigate the differences in underlying neural mechanisms of semantic processing in youths with ASD, their unaffected siblings, and typically developing (TD) youths. Endophenotypes for ASD were defined as similarly heritable traits that were correlated with ASD. This study recruited 39 ASD youths (mean age = 14.8 years, standard deviation [SD] = 3.9 years), their unaffected siblings (mean age = 15.7 years, SD= 5.2 years), and 40 TD youths (mean age = 14.6 years, SD= 4.7 years). These three groups of participants were matched with IQ, age, and handedness. Participants were instructed to judge whether two Chinese characters were related in meaning in an MRI scanner. Our behavioral result showed that there were no significant differences on accuracy and reaction time among these three groups. Brain imaging data revealed that unaffected siblings and TD youths showed greater brain activation in the left MTG as compared with ASD youths. Moreover, the unaffected siblings and ASD youths showed greater cuneus activation as compared to TD youths. Furthermore, unaffected siblings showed intermediate left IFG activation between TD and ASD youths, with the strongest activation in TD youths and the weakest in ASD youths. Our findings provided a supportive evidence that abnormal neural activation in the left IFG and the cuneus during semantic processing could serve as an endophenotype of ASD. For our unaffected ASD siblings, they may have intact lexical representation system as TD youths; however, because of shared genetic features with ASD, they adpoted the same perception-based strategies as ASD youths, and may have rather immature ability to manipulate semantic representations.
Книги з теми "Neural mechanisms autism"
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Westberg, Lars, and Hasse Walum. Oxytocin and Vasopressin Gene Variation and the Neural Basis of Social Behaviors. Edited by Turhan Canli. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.011.
Повний текст джерелаАнотація:
Experimental studies in rodents and humans show that the neuropeptides oxytocin and vasopressin are important regulators of behaviors related to social interactions. Evidence for positive effects of oxytocin treatment on symptoms of psychiatric disorders characterized by impaired social functioning has emerged. Numerous studies report associations between various social behaviors, the risk of autism, and polymorphisms inOXTRandAVPR1A. This chapter provides an overview of these genetic association studies. Although many of the published findings are inconclusive and need replication in independent samples, the chapter concludes that variants ofOXTRandAVPR1Aseem to moderate individual variation in different aspects of social behavior. The challenges for future studies include replication of current findings, identification of the functional variants, and characterization of the neural mechanisms mediating the gene-behavior associations, as well as exploration of the pharmacogenetic potential ofOXTRandAVPR1Ain future clinical trials.
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Patisaul, Heather B., and Scott M. Belcher. Endocrine Disruptors and Neurobehavioral Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780199935734.003.0006.
Повний текст джерелаАнотація:
This chapter focuses on the role environmental pollutants are playing in the rapidly rising rate of neurodevelopmental disorders in children. The available EDC data are summarized and analyzed in relation to whether or not evidence supports a role for EDCs as contributing to neural disorders. The distinction between endocrine disruption and neurotoxicity is established by focusing on the differences between toxicants, toxins, and altered endocrine/neuroendocrine effects in organizational alterations of the brain. Evidence from experimental systems demonstrating effects of EDCs on the developing brain and the potential roles for EDCs as bad actors in rising rates of autism spectrum disorder (ASD), and attention deficit hyperactivity disorder (ADHD) are presented in detail. Additional impacts of EDCs on neurodegenerative disorders, including Parkinsons’s disease, are reviewed. The mechanisms of rotenone and paraquat neurodegeneration are compared and contrasted with the evidence and mechanisms of actions for organochlorine and organophosphate pesticides in Parkinsons’s disease.
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Beauchaine, Theodore P., and Sheila E. Crowell, eds. The Oxford Handbook of Emotion Dysregulation. Oxford University Press, 2018. http://dx.doi.org/10.1093/oxfordhb/9780190689285.001.0001.
Повний текст джерелаАнотація:
Emotion dysregulation—which is often defined as the inability to modulate strong affective states including impulsivity, anger, fear, sadness, and anxiety—is observed in nearly all psychiatric disorders. These include internalizing disorders such as panic disorder and major depression, externalizing disorders such as conduct disorder and antisocial personality disorder, and various other disorders including schizophrenia, autism, and borderline personality disorder. Among many affected individuals, precursors to emotion dysregulation appear early in development, and often predate the emergence of diagnosable psychopathology. Collaborative work by Drs. Crowell and Beauchaine, and work by many others, suggests that emotion dysregulation arises from both familial (coercion, invalidation, abuse, neglect) and extrafamilial (deviant peer group affiliations, social reinforcement) mechanisms. These studies point toward strategies for prevention and intervention. The Oxford Handbook of Emotion Dysregulation brings together experts whose work cuts across levels of analysis, including neurobiological, cognitive, and social, in studying emotion dysregulation. Contributing authors describe how early environmental risk exposures shape emotion dysregulation, how emotion dysregulation manifests in various forms of mental illness, and how emotion dysregulation is most effectively assessed and treated. This is the first text to assemble a highly accomplished group of authors to address conceptual issues in emotion dysregulation research; define the emotion dysregulation construct at levels of cognition, behavior, and social dynamics; describe cutting-edge assessment techniques at neural, psychophysiological, and behavioral levels of analysis; and present contemporary treatment strategies. Conceptualizing emotion dysregulation as a core vulnerability to psychopathology is consistent with modern transdiagnostic approaches to diagnosis and treatment, including the Research Domain Criteria and the Unified Protocol, respectively.
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Gaitanis, John, Phillip L. Pearl, and Howard Goodkin. The EEG in Degenerative Disorders of the Central Nervous System. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0013.
Повний текст джерелаАнотація:
Nervous system alterations can occur at any stage of prenatal or postnatal development. Any of these derangements, whether environmental or genetic, will affect electrical transmission, causing electroencephalogram (EEG) alteration and possibly epilepsy. Genetic insults may be multisystemic (for example, neurocutaneous syndromes) or affect only the brain. Gene mutations account for inborn errors of metabolism, channelopathies, brain malformations, and impaired synaptogenesis. Inborn errors of metabolism cause seizures and EEG abnormalities through a variety of mechanisms, including disrupted energy metabolism (mitochondrial disorders, glucose transporter defect), neuronal toxicity (amino and organic acidopathies), impaired neuronal function (lysosomal and peroxisomal disorders), alteration of neurotransmitter systems (nonketotic hyperglycinemia), and vitamin and co-factor dependency (pyridoxine-dependent seizures). Environmental causes of perinatal brain injury often result in motor or intellectual impairment (cerebral palsy). Multiple proposed etiologies exist for autism, many focusing on synaptic development. This chapter reviews the EEG findings associated with this myriad of pathologies occurring in childhood.
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Friston, Karl J., and Raymond J. Dolan. Computational Psychiatry and the Bayesian Brain. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0072.
Повний текст джерелаАнотація:
This chapter considers recent advances in computational neuroscience that are especially relevant for psychiatry. We offer a review of computational psychiatry in terms of its ambitions, emerging domains of application, and promises for the future. Our focus is on theoretical formulations of brain function that accommodate subjective beliefs and behavior within formal (computational) frameworks—frameworks that can be grounded in neurophysiology down to the level of synaptic mechanisms. Understanding the nature and principles that underlie functional brain architectures is, we assume, essential for understanding and phenotyping psychopathology and its pathophysiological underpinnings. To illustrate computational approaches to psychiatric disorders, we focus on active (Bayesian) inference and predictive coding. Specifically, we try to explain how the basic principles of neuronal computation are being used to understand psychiatric phenomena, ranging from affiliative behavior and theory of mind in autism to abnormalities of smooth pursuit eye movements in schizophrenia.
Частини книг з теми "Neural mechanisms autism"
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Anagnostou, Evdokia, Deepali Mankad, Joshua Diehl, Catherine Lord, Sarah Butler, Andrea McDuffie, Lisa Shull, et al. "Neural Mechanisms in Autism." In Encyclopedia of Autism Spectrum Disorders, 1994–2007. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1698-3_572.
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Casanova, Manuel. "Neural Mechanisms in Autism." In Encyclopedia of Autism Spectrum Disorders, 3102–15. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-91280-6_572.
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Ibrahim, Karim, Gregory McCarthy, and Denis G. Sukhodolsky. "Neural Mechanisms of Emotional Dysregulation." In Encyclopedia of Autism Spectrum Disorders, 1–4. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4614-6435-8_102453-1.
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Ibrahim, Karim, Gregory McCarthy, and Denis G. Sukhodolsky. "Neural Mechanisms of Emotional Dysregulation." In Encyclopedia of Autism Spectrum Disorders, 3115–17. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-91280-6_102453.
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Folstein, Susan E., Michael Dowd, Raymond Mankoski, and Ovsanna Tadevosyan. "How Might Genetic Mechanisms Operate in Autism?" In Autism: Neural Basis and Treatment Possibilities, 70–83. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470869380.ch5.
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Nakai, Nobuhiro, Eric T. N. Overton, and Toru Takumi. "Optogenetic Approaches to Understand the Neural Circuit Mechanism of Social Deficits Seen in Autism Spectrum Disorders." In Advances in Experimental Medicine and Biology, 523–33. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-8763-4_36.
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Hirsch, Emily, and Leslie Hulvershorn. "Neural Findings in Pediatric Irritability." In Irritability in Pediatric Psychopathology, edited by Amy Krain Roy, Melissa A. Brotman, and Ellen Leibenluft, 171–94. Oxford University Press, 2019. http://dx.doi.org/10.1093/med-psych/9780190846800.003.0009.
Повний текст джерелаАнотація:
Irritability has been conceptualized as a clinical phenomenon that cuts across various psychiatric disorders. Moreover, it is one of the most common reasons that children and adolescents present for mental health treatment. Despite the high prevalence and impairment associated with irritability, until recently, relatively little was known about the brain mechanisms underlying it. Understanding more about the neural mechanisms associated with irritability will likely enhance treatment development. In this chapter, the authors synthesize research that has characterized aspects of irritability in children and adolescents who are typically developing and in those with psychiatric disorders, including severe mood dysregulation (SMD), disruptive mood dysregulation disorder (DMDD), bipolar disorder, and disruptive behavior disorders, as well as attention deficit/hyperactivity disorder and autism, and they suggest future directions for research in this area.
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Friedman, Hagit. "Autism Spectrum Disorder (ASD): From Molecular Mechanism to Novel Therapeutic Approach." In Learning Disabilities - Neurobiology, Assessment, Clinical Features and Treatments. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.100537.
Повний текст джерелаАнотація:
Autism spectrum disorder (ASD) is the joint name for neurodevelopmental impairments characterized by abnormal social interaction, communication difficulties, limited range of activities and areas of interest, and typical motor impairments. There is a remarkable increase in the prevalence of ASD over the past 30 years. Studies indicate that genetic, neurological, and environmental factors are involved in the emergence of ASD, and recent works describe the neuromolecular mechanism implicated in the basis of ASD. 3LT has now developed into a therapeutic procedure that is used for three main goals: to reduce inflammation, edema, and chronic orthopedic disorders; to promote healing of wounds, deeper tissues, and nerves; and to treat neurological injuries and pain. 3LT may treat neurological injuries by lowering levels of inflammation proteins and by stimulation of mitochondria to increase the production of adenosine triphosphate and neural growth factors. This review aims to discuss the current evidence for the effects and mechanisms of 3LT at the cellular level and the effects of 3LT-induced changes in brain development and function. Early and effective intervention, through the developmental time window of high ASD susceptibility, using tools that are directed to the mechanism of pathology, may minimize neurological and functional deficits.
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Christian, Kimberly M., Song Hongjun, and Ming Guo-li. "Application of Stem Cells to Understanding Psychiatric Disorders." In Neurobiology of Mental Illness, edited by Karl Deisseroth, 123–26. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199934959.003.0009.
Повний текст джерелаАнотація:
Due to the remarkable discovery that somatic cells from adult humans could be reprogrammed into pluripotent stem cells, we now have the opportunity to create renewable sources of human neurons and glial cells to investigate the mechanisms underlying psychiatric disease. These induced stem cells are genetically identical to the donor individual and allow an unprecedented opportunity to investigate neurodevelopmental and neurodegenerative processes in a genetic context known to be permissive for disease. Although many higher-order features of mental disorders are inaccessible in cellular and animal models, we can gain insight into causal mechanisms underlying dysregulated neural circuitry by characterizing the functional capacity of human neurons in different environmental and genetic contexts. The field is now in its infancy and researchers are just beginning to explore the phenotypes of neurons derived from patients with complex psychiatric disorders such as schizophrenia and autism. Here we review some of the major breakthroughs and significant challenges in the effort to leverage this resource to develop innovative therapeutic strategies for psychiatric disease.
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Sagata, Noriaki, Yasunari Sakai, and Takahiro A. Kato. "Clarifying the Pathophysiological Mechanisms of Neuronal Abnormalities of NF1 by Induced-Neuronal (iN) Cells from Human Fibroblasts." In Neurofibromatosis [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98817.
Повний текст джерелаАнотація:
Direct conversion techniques, which generate induced-neuronal (iN) cells from human fibroblasts in less than two weeks, are expected to discover unknown neuronal phenotypes of neuropsychiatric disorders. Here, we present unique gene expression and cell morphology profiles in iN cells derived from neurofibromatosis type 1 (NF1) patients. NF1 is a single-gene multifaceted disorder with relatively high co-occurrence of autism spectrum disorder (ASD). Adenylyl cyclase (AC) dysfunction is one of the candidate pathways in abnormal neuronal development in the brains of NF1 patients. In our study, microarray-based transcriptomic analysis of iN cells from healthy controls (males) and NF1 patients (males) revealed significantly different gene expression of 149 (110 were upregulated and 39 were downregulated). In iN cells derived from NF1 patients (NF1-iN cells), there was a change in the expression level of 90 genes with the addition of forskolin, an AC activator. Furthermore, treatment with forskolin dramatically changed the cell morphology, especially that of NF1-iN cells, from flat-form to spherical-form. Current pilot data indicate the potential therapeutic effect of forskolin or AC activators on neuronal growth in NF1 patients. Further translational research is needed to validate the pilot findings for future drug development of ASD.
Тези доповідей конференцій з теми "Neural mechanisms autism"
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Nikolaeva, Elena I. "Genetics and psychophysiology of ADHD and autism." In 2nd International Neuropsychological Summer School named after A. R. Luria “The World After the Pandemic: Challenges and Prospects for Neuroscience”. Ural University Press, 2020. http://dx.doi.org/10.15826/b978-5-7996-3073-7.12.
Повний текст джерелаАнотація:
The paper discusses the brain mechanisms of autism and attention deficit hyperactivity disorder. It is shown that these disorders are associated with different genetic causes that create certain psychophysiological mechanisms. Nevertheless, their diagnosis is interrelated. Moreover, a child is often first diagnosed with ADHD, and then the diagnosis is changed to “autism spectrum disease”. Among the most common causes of the disease is the behavior of retrotransposons. Retrotransposons (also called transposons via intermediate RNA) are genetic elements that can amplify themselves in the genome. These DNA sequences use a “copy and paste” mechanism, whereby they are first transcribed into RNA and then converted back to identical DNA sequences via reverse transcription, and these sequences are then inserted into the genome at target sites. In humans, retro elements take up 42 % of the DNA. The conclusion is made that for the formation of an individual profile of gene expression in the neuron, the most important is the phenomenon of somatic mosaicism, due to the process of L1 retrotransposition, in addition to the classical described mechanisms of differentiation. The number of such events and their localization is significant as they are likely to contribute to the development of both autism and ADHD.