Relevant bibliographies by topics / Autism – Etiology

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  2. Dissertations / Theses
  3. Books
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Academic literature on the topic 'Autism – Etiology'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 April 2022

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Journal articles on the topic "Autism – Etiology"

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Cammisa, Kathryne M., and Stephen H. Hobbs. "Etiology of Autism." Occupational Therapy in Mental Health 12, no. 2 (June 4, 1993): 39–67. http://dx.doi.org/10.1300/j004v12n02_03.

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Folstein, Susan E., and Joseph Piven. "Etiology of Autism: Genetic Influences." Pediatrics 87, no. 5 (May 1, 1991): 767–73. http://dx.doi.org/10.1542/peds.87.5.767.

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Infantile autism was first described by Kanner in 1943.1 Based on the observation that symptoms often began shortly after birth and always by two or three years of age, Kanner believed that autism was caused by an unknown, inborn defect. Because this syndrome was so severe and peculiar, it seemed unlikely to be an understandable outcome of a child's life experiences. In the years since Kanner first described this disorder, research findings have supported his initial interpretations. It is now generally accepted that autism has a biologic cause, and considerable research has been carried out with the aim of uncovering its nature. Both hereditary factors and the prenatal and perinatal environment have been considered. This paper will review the role of genetic factors in the cause of autism; the role of the prenatal and perinatal environment is considered in the paper by Nelson.51 Three types of genetic associations have been described: (1) the familial aggregation of autism, per se—autism is more common in the sibs of affected children; (2) the familial aggregation of other disorders in the family members of autistic children—a variety of disorders that are mild, but probably conceptually related, have recently been described in relatives; and (3) autism appears in association with a few particular disorders of known genetic etiology. FAMILIAL AGGREGATION OF AUTISM Population and Family Studies In most case series and a few population-based studies, the prevalence of autism in the siblings of autistic children has been estimated to be about 2% to 3%.2,3 While this number is small, it is 50 to 100 times greater than the expected rate of autism of 4 to 5 per 10 000 in the population.4,5
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Hnilicova, Silvia, Katarina Babinska, Hana Celusakova, Diana Filcikova, Petra Kemenyova, and Daniela Ostatnikova. "AUTISM ETIOLOGY, SCREENING AND DIAGNOSIS." Pathophysiology 25, no. 3 (September 2018): 193–94. http://dx.doi.org/10.1016/j.pathophys.2018.07.079.

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Mohammadi, Mohammad-Reza, and Shahin Akhondzadeh. "Autism Spectrum Disorders: Etiology and Pharmacotherapy." Current Drug Therapy 2, no. 2 (May 1, 2007): 97–103. http://dx.doi.org/10.2174/157488507780619095.

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Nelson, Karin B. "Prenatal and Perinatal Factors in the Etiology of Autism." Pediatrics 87, no. 5 (May 1, 1991): 761–66. http://dx.doi.org/10.1542/peds.87.5.761.

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This paper will review studies on prenatal and perinatal factors and the etiology of autism. It will focus on whether identified risk factors have been consistent from report to report, the extent to which identified risk factors are likely to be causal, and the extent to which identification of these factors can contribute to the development of strategies for the prevention of autism. Autism is one of a group of disorders often described as the developmental disabilities. Other disorders in this group are mental retardation, cerebral palsy, epilepsy, and learning disorders. Like these other disorders, autism is delineated by a set of observable dysfunctions and to some extent also by a shared natural history. Like these other disorders, autism is not a disease in the sense of having known biologic markers or known major etiologic factors in common. It is probable that autism is not the result of a single etiologic factor. Before examining the literature on autism, it may be useful to consider briefly what is known about maternal, pregnancy, and birth factors in the other developmental disabilities. EXPERIENCE WITH OTHER DEVELOPMENTAL DISABILITIES Contrary to expectations based on a hypothetical "continuum of reproductive causality," different developmental disabilities often have different major predictors. For example, the major known predictors of mental retardation and learning disorders are family characteristics such as educational level of the parents and measures of socioeconomic status.1,2 These characteristics are not important risk factors for cerebral palsy3 or epilepsy.4,5 Low birth weight is related to cerebral palsy but not to epilepsy in persons without cerebral palsy.6
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Ring, Aliza, Yoram Barak, Aharon Ticher, Israel Ashkenazi, Avner Elizur, and Abraham Weizman. "Evidence for an infectious etiology in autism." Pathophysiology 4, no. 2 (June 1997): 91–96. http://dx.doi.org/10.1016/s0928-4680(97)00168-5.

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Bushwick, Nathaniel Lewis. "Social learning and the etiology of autism." New Ideas in Psychology 19, no. 1 (April 2001): 49–75. http://dx.doi.org/10.1016/s0732-118x(00)00016-7.

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Wachtel, L. E. "Catatonia in autism: Etiology, incidence and treatment." European Psychiatry 23 (April 2008): S402. http://dx.doi.org/10.1016/j.eurpsy.2008.01.1391.

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Sundberg, Mark L. "The Search for the Etiology of Autism." Analysis of Verbal Behavior 20, no. 1 (April 2004): 3–4. http://dx.doi.org/10.1007/bf03392987.

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Hall, Genae A. "Towards a Balanced Account of Autism Etiology." Analysis of Verbal Behavior 20, no. 1 (April 2004): 37–43. http://dx.doi.org/10.1007/bf03392991.

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Dissertations / Theses on the topic "Autism – Etiology"

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Harrison, Lucy. "Autism: the etiology and treatments of the disorder." Thesis, Boston University, 2004. https://hdl.handle.net/2144/27668.

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Boston University. University Professors Program Senior theses.
PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
2031-01-02
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Nazeen, Sumaiya. "Integrative analysis of heterogeneous genomic datasets to discover genetic etiology of autism spectrum disorders." Thesis, Massachusetts Institute of Technology, 2014. http://hdl.handle.net/1721.1/93836.

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Thesis: S.M., Massachusetts Institute of Technology, Department of Electrical Engineering and Computer Science, 2014.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 99-109).
Understanding the genetic background of complex diseases is crucial to medical research, with implications to diagnosis, treatment and drug development. As molecular approaches to this challenge are time consuming and costly, computational approaches offer an efficient alternative. Such approaches aim at predicting and prioritizing genes for a particular disease of interest. State-of-the-art gene prediction and prioritization methods rely on the observation that disease-causing genes have some sort of functional similarity based on either sequence, phenotype, protein-protein interaction (PPI) network, or functional annotation. Another increasingly accepted view is that human diseases result from perturbations of molecular networks, and genes causing the same or similar diseases tend to be close to one another in molecular networks. Such observations have built the basis for a large collection of computational approaches to find previously unknown genes associated with certain diseases. The majority of the methods are designed based on protein interactome networks, with integration of other large-scale omics data, to infer how likely it is that a gene is associated with a disease. In this thesis, we set out to address this outstanding challenge of understanding the genetic etiology of autism spectrum disorder (ASD), which refers to a group of complex neurodevelopmental disorders sharing the common feature of dysfunctional reciprocal social interaction. We introduce three novel methods for computing how likely a given gene is to be involved in ASDs based on copy number variations (CNVs), phenotype similarity, and protein interactome network topology. We also customize a random walk with restarts algorithm for ASD gene prioritization for the first time. Finally, we provide a novel integrative approach for combining CNV, phenotype similarity, and topology-related information with existing knowledge from literature. Our integrative approach outperforms the individual schemes in identifying and ranking ASD related genes. Our candidate gene set provides a number of interesting biological insights in that it is overrepresented in a number of interesting signaling, cell-adhesion and neurological pathways, molecular functions, and biological processes that are worth further investigation in connection with ASDs. We also find evidence for an interesting connection between gastrointestinal disorders, particularly inflammatory bowel diseases (IBD), and ASDs. The subnetworks we identify indicate the possibility of existence of subclasses of disorders along the autism spectrum.
by Sumaiya Nazeen.
S.M.
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Miemczyk, Stefan. "Towards the identification of environmental exposures and epigenetic marks related to the etiology of Autism." Thesis, Linköpings universitet, Biologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-138946.

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Autism is a complex disorder with possible genetic, epigenetic and environmental components. As the etiology remains uncertain and an increase in incidence is suspected, the involvement of possible environmental risk factors has gained increasing attention. With this thesis, I aim to provide tools for assessing such risk factors. Firstly, I aim to construct a questionnaire for the analysis of an environmental component in the etiology of autism. Secondly, I aim to assess the importance of prenatal exposure to metals in certain diseases and thirdly I aim to construct a methodology enabling the analysis of the mitochondrial epigenome, which is especially interesting in relation to autism as mitochondrial diseases occur more frequently in an autistic population than in the general population. For the creation of the questionnaire the scientific literature was reviewed. The resulting questionnaire contains general, prenatal, neonatal and paternal risk factors. The metal analysis was conducted on the cord blood of patients who later developed autism, antinuclear antibodies positive rheumatoid arthritis or diabetes, which were then compared to healthy control subjects. My findings propose a link between elevated levels of cord blood cadmium or aluminum and rheumatic arthritis. In addition, elevated aluminum levels might be associated with autism. In regards to the analysis of the mitochondrial epigenome, to my knowledge, no standard protocol exists with frozen human whole blood as a source. In this thesis, I succeeded in creating the basis for such a protocol, however still needing several small modifications for an increased overall yield.
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Wong, Dana. "Theory of mind and executive function impairments in autism spectrum disorders and their broader phenotype : profile, primacy and independence." University of Western Australia. School of Psychology, 2004. http://theses.library.uwa.edu.au/adt-WU2004.0066.

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Impairments in both theory of mind (ToM; the ability to attribute mental states to oneself and others) and executive function (EF; a group of high-level cognitive functions which help guide and control goal-directed behaviour) have been demonstrated in individuals with autism spectrum disorders (ASDs). Both deficits have been proposed by different groups of researchers as being the single primary cognitive deficit of autism, which can subsume the other deficit as secondary or artefactual. However, few studies have examined the nature of the relationship between ToM and EF in ASDs or conducted a systematic investigation of their relative primacy. This research principally sought to establish the primacy and independence of impairments in ToM and EF in ASDs and thereby evaluate the validity of single versus multiple primary deficit models of autism. These aims were addressed in two studies, both broad in scope. The first study was an investigation of the profile, primacy, and independence of ToM and EF impairments in individuals with ASDs. The sample included 46 participants with ASDs and 48 control participants matched on age and non-verbal ability. The profile of impairments was examined by measuring ToM and a range of EF components using tasks employing, wherever possible, process-pure indices of performance. Primacy was measured by focussing on i) whether or not the deficits observed were universal among individuals with ASDs; ii) whether the deficits were able to discriminate individuals with ASDs from matched controls (i.e., predict group membership); and iii) the ability of ToM and EF deficits to explain the full range of autistic symptomatology, as measured by correlating cognitive performances with behavioural indices. The relationship between ToM and EF impairments was investigated by conducting correlations between ToM and EF variables as well as analysing the incidence of dissociations between impairments in the two domains. The ASD group was found to demonstrate significant impairments in ToM and several components of EF including planning, verbal inhibition, working memory (in a context where inhibitory control was required), and both verbal and non-verbal generativity. However, neither ToM nor EF impairments were able to meet all of the criteria for a primary deficit in ASDs. EF deficits were found to be more primary, but could not account for ToM as a secondary deficit, as ToM and EF were found to be independent (i.e., uncorrelated and dissociable) deficits in the ASD group. This pattern of results suggested that a multiple deficits model involving at least two independent impairments appeared to best characterise ASDs, but the data were compatible with several variants of such a model (e.g., involving distinct subtypes versus a multidimensional spectrum). The second study was an investigation of ToM and EF impairments in siblings of individuals with ASDs, who have previously been found to demonstrate a subclinical “broad autism phenotype”. The main aims of this study were i) to identify whether ToM or EF deficits could meet criteria for an “endophenotype” or vulnerability marker for the autism genotype in unaffected relatives, which would have further implications about the primacy of ToM and EF in ASDs; and ii) to further investigate the validity of various multiple deficits models of ASDs by examining the pattern of ToM and EF performance in those showing the broad phenotype. Participants were 108 siblings of individuals with ASDs and 67 siblings of controls, tested on the same ToM and EF tasks used in the first study. Confirming the superior primacy of EF deficits found in Study One, there was no significant difference in ToM performance between ASD and control siblings, but ASD siblings showed weaknesses on two measures of EF. Furthermore, there appeared to be different subgroups of siblings demonstrating different cognitive profiles, consistent with the heterogeneity evident in the first study. This research indicated that ASDs cannot be explained by a single primary cognitive deficit. These findings hold important theoretical and empirical implications and highlight further questions about which type of multiple deficits model might best explain ASDs.
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Whitaker, Ashley Lorraine. "Seek and Destroy| A Heuristic Self-Search Inquiry on the Etiology of Existential Injury in Autism Spectrum Disorder and Turner Syndrome." Thesis, Saybrook University, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10688746.

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This heuristic self-search inquiry (Sela-Smith, 2001, 2002) study reviews empirical and theoretical research on Autism Spectrum Disorder (Asperger, 1938, 1944; Bleuler, 1910, 1911a, 1911b; Kanner, 1943) and Turner Syndrome (Funke, 1902; Turner, 1938; Ullrich, 1930). It conjoins with existing literature on the main principles of existential-humanistic psychology and psychotherapy to prompt a heuristic investigation of the problem of the researcher-participant’s veridical reference as it pertains to her subjective experience. The purpose of the study was to elucidate the complementarity of what the existential-humanistic literature refers to as the intelligible responses of her equiprimordial I-who-feels encounter with biopsychological trauma as an initiator of chronic existential injury as an adult diagnosed with a conglomerate of associated clinical symptoms to sketch out their possible existential etiologies.

Stimuli precipitating heuristic data collection included psychotherapy sessions, childhood medical records, medical examinations and consultations conducted during the study, and prior academic work. The heuristic data collection adhered to Moustakas’ (1990) phases and processes of research. Schneider’s (2008/2015) expansion-constriction continuum model of consciousness of six-domains (physiological, environmental, cognitive, psychosexual, interpersonal, and experiential) was used to analyze the heuristic data and decipher whether tacit knowledge of the researcher-participant’s I-who-feels experience was discovered in the inquiry. A Heuristic-Expansion-Constriction Change scale was designed to subjectively measure degree of change in each domain. Bronfenbrenner’s (1979) biosystemic model of human development was employed to conceptualize the etiology of existential injury across four systems of being: the microsystem, mesosystem, ectosystem, and macrosystem.

The heuristic research findings indicated a high degree of meta-level abstraction in the researcher-participant paralleled by the review of the literature. Populations experiencing recalcitrant complications of similar ilk might gain insight into their psychological etiologies of by, through self-examination and change, acknowledging resistance to the I-who-feels . Additionally, ongoing interdisciplinary intervention by an established care team providing medical and psychotherapeutic support might prove satisfactorily beneficial. Data was distilled into a series of recommendations that existential-humanistic psychotherapists might adopt when working with clients exhibiting chronic existential injury due to multiplex medical symptoms. Implications for these populations were subsequently discussed, with special recommendations provided for medical providers on addressing existential concerns in patients.

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Schutz, Christopher Kevin. "Genetic analysis of complex neurodevelopmental disorders : a model for the genetic etiology of autism and the related pervasive developmental disorders and mapping of a gene responsible for x-linked mental retardation /." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0003/NQ42764.pdf.

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Carlton, Rashad. "The Association between the Measles, Mumps, and Rubella Vaccine and the Development of Autism: A Meta-Analysis." [Tampa, Fla] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002301.

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ADDOU, MANSOUR. "Autisme infantile precoce : etude des facteurs etiologiques a propos de huit observations et analyse d'un symptome chez un enfant autiste." Besançon, 1991. http://www.theses.fr/1991BESA3056.

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Rego, Sara Weisz Sampaio Estrela. "Autismo: fisiopatologia e biomarcadores." Master's thesis, Universidade da Beira Interior, 2012. http://hdl.handle.net/10400.6/1167.

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Perturbações do espectro autista é o termo usado para identificar um grupo de alterações invasivas do desenvolvimento caracterizadas por défices na socialização e comunicação e por comportamentos bizarros e repetitivos. Esta classificação inclui o Autismo, o Síndrome de Asperger e a Perturbação Global do Desenvolvimento Sem Outra Especificação [1]. Leo Kanner em 1943 e Hans Asperger em 1944 foram possivelmente os primeiros a descrever o tipo de distúrbios englobados nesta categoria, destacando a especificidade do défice de interação social que tem sido, desde então, considerado o sintoma principal do autismo [2]. A prevalência do autismo situa-se entre 10 e 20 casos por cada 10000 crianças e tem vindo a aumentar significativamente desde a década de 1960 sendo este aumento justificado pelo maior reconhecimento desta doença como problema de saúde pública e ainda pelas constantes mudanças na prática dos mesmos. Os sintomas clínicos estão usualmente presentes aos três anos, contudo o défice no desenvolvimento da linguagem atrasa a sua identificação [2,3]. As Perturbações do Espectro Autista são fortemente genéticas e multifatoriais, havendo interação entre muitos fatores de risco [3]. Há uma incessante procura de marcadores biológicos para o Autismo, ou seja, indicadores mensuráveis em simples amostras biológicas que podem ser utilizados como fatores de risco, indicadores diagnósticos e podem ainda ajudar na elaboração do plano de tratamento mais adequado [1]. O objetivo deste trabalho passa por fazer uma revisão e sistematização sobre o autismo e os seus biomarcadores, estudando os benefícios clínicos e diagnósticos de cada um. Através da evolução destes estudos pretende-se ainda perspetivar o futuro desta patologia. A pesquisa bibliográfica foi realizada através das bases de dados: Medline/PubMed, Medscape, E-medicine assim como vários livros de referência sobre a especialidade. Esta pesquisa foi realizada em português e inglês. Após uma pesquisa detalhada foi possível concluir que as Perturbações do Espectro Autista apresentam inúmeros fatores causais, sendo ainda uma área de investigação com muitos desafios a enfrentar. O perfil genético e metabólico, o perímetro cefálico, a estrutura e fisiologia cerebral, entre muitos outros, são exemplos de biomarcadores propostos para o autismo. Apesar da grande evolução das técnicas e metodologias de estudo do autismo e da melhoria na sua compreensão científica, pouco se tem conseguido no que toca a traduzir os biomarcadores em evidências clínicas.
Autism spectrum disorder is used for a diverse group of developmental conditions characterized by impairments in social skills and communication and repetitive or unusual behaviors. This classification includes Autism, Asperger’s syndrome and Pervasive Developmental Disorder not otherwise specified [1]. Leo Kanner (1943) and Hans Asperger (1944) were possibly the first ones to describe the type of empathy disorders encompassed in this category, highlighting the specificity of the social interaction deficit which has, ever since, been regarded as the core symptom of Autism [2]. Autistic disorder’s prevalence is between 10 and 20 per 10 000 children and apparently has greatly increased since 1960’s. This is justified by its recognition as a public health problem and also by changes made in policy and practice. Clinical signs are usually present at the age of 3 years, but impairments in language development might delay identification of these symptoms [2,3]. Autism spectrum disorders are highly genetic and multifactorial, with many risk factors acting together [3]. There is constant search for Autism’s biological markers, which are defined as measurable indicators in simple biological samples. They can be used as risk factors, diagnostic indicators and even help planning the most appropriate treatment [1]. The aim of this work is to review and systematize Autism and its biomarkers, studying both the clinical and diagnostic benefits of each one of them. Through the evolution of these studies, we also intend to look at the future of this pathology. The literature search was performed using the following databases: Medline/PubMed, Medscape, E-medicine as well as several reference books on the specialty. This research was conducted both in Portuguese and English. After a detailed research a conclusion was made that Autism Spectrum Disorders have several causal factors and it is an area of investigation with many challenges. The genetic and metabolic profile, head circumference, brain structure and many others, are possible biomarkers for autism. Despite great development and understanding of the techniques and methodologies, little has been achieved with regard to translate biomarkers on clinical evidence.
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Chang, Bryant Duy. "Prevalence, etiology, and treatment of sleep disorders in autism spectrum disorder." Thesis, 2019. https://hdl.handle.net/2144/36640.

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BACKGROUND: Autism Spectrum Disorder is a range of neurodevelopmental disorders that typical manifest as social deficits, delayed or impaired communication skills, and repetitive behaviors in day-to-day life. Patients with Autism Spectrum Disorder (ASD) often present with other concurrent clinical disorders. Sleep disorders (SD) and sleep issues are highly prevalent in ASD children and rank as one of the most common concurrent clinical disorders. Prevalence rates vary widely, ranging from 40 to 80 percent, as compared with that of typically developing children in which prevalence rates are approximately 30 percent. Sleep problems can have an impact on daytime health and may result in neurocognitive dysfunction and behavioral disruptions. A cyclical pattern arises: individuals with autism are observed to have sleep difficulties, which may exacerbate autistic traits, which can in turn further worsen their quality of sleep. Therefore, sleep disorders may have wide ranging effects on daytime functioning, developmental progress, and quality of life for children with ASD. OBJECTIVES: The purpose of this thesis is to provide a review of the research status of ASD, SD, the interplay between these two disorders, and therapeutic interventions that have been researched or are currently being investigated. A goal of this thesis is also to recommend areas of future investigation based on the current state of autism research. METHODS: A literature review of studies, abstracts, and clinical trial data relating to ASD, SD, and other comorbidities observed in ASD was performed. CONCLUSION: Current models and theories on the relationship between ASD and SD suggest that the underlying etiology of autism itself may contribute to sleep troubles, and might even have wide-reaching impacts on other unrelated aspects of ASD. Gastrointestinal, otolaryngologic, and psychiatric comorbidities are observed in autism and may affect sleep in these patients, but the mechanism by which this occurs is unclear. There are many treatments for sleep troubles in ASD such as melatonin and behavioral interventions, with varying success. Much work is required to understand the underlying mechanism between both autism and sleep disorders. There is also a need for more efficacious therapeutic interventions, but there are multiple clinical trials underway which may have promising results. Future studies should also incorporate robust data-collection instruments such as polysomnography to validate findings.
2021-06-14T00:00:00Z
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Books on the topic "Autism – Etiology"

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(Firm), Thomson Gale, ed. Why is autism on the rise? Farmington Hills, Mich: Greenhaven Press, a part of Gale, Cengage Learning, 2014.

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D, Oller Stephen, ed. Autism: The diagnosis, treatment & etiology of the undeniable epidemic. Sudbury, Mass: Jones and Bartlett, 2010.

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Waldman, Michael. Does television cause autism? Cambridge, Mass: National Bureau of Economic Research, 2006.

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H, Dunn Denise, ed. Allergies and autism. New York: Nova Science, 2010.

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1950-, Gillberg Christopher, ed. The biology of the autistic syndromes. New York: Praeger, 1985.

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Dochniak, Michael J. Allergies and autism. Hauppauge, N.Y: Nova Science, 2009.

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Dochniak, Michael J. Allergies and autism. Hauppauge, N.Y: Nova Science, 2009.

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The autism puzzle: Connecting the dots between environmental toxins and rising autism rates. New York, NY: Seven Stories Press, 2011.

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Autism and post-traumatic stress disorder: Ending autistic fixation. Springfield, Ill: Charles C. Thomas, 2000.

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1950-, Gillberg Christopher, and Gillberg Christopher 1950-, eds. The autisms. 4th ed. New York: Oxford University Press, 2012.

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Book chapters on the topic "Autism – Etiology"

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Steffenburg, Suzanne, and Christopher Gillberg. "The Etiology of Autism." In Diagnosis and Treatment of Autism, 63–82. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-0882-7_6.

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Durand, V. Mark. "Etiology." In Autism spectrum disorder: A clinical guide for general practitioners., 37–56. Washington: American Psychological Association, 2014. http://dx.doi.org/10.1037/14283-002.

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Gardener, Hannah, and Kristen Lyall. "Perinatal and Neonatal Complications in Autism Etiology." In Comprehensive Guide to Autism, 3–25. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-4788-7_76.

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Hassan, Wassim. "Anime, Manga, and the Etiology of Autism." In Encyclopedia of Autism Spectrum Disorders, 1–3. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-6435-8_102533-1.

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Hassan, Wassim. "Anime, Manga, and the Etiology of Autism." In Encyclopedia of Autism Spectrum Disorders, 223–25. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-91280-6_102533.

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van Steensel, Francisca Johanna Arnoldina, Susan Maria Bögels, Iliana Magiati, and Sean Perrin. "Anxiety in Individuals with ASD: Prevalence, Phenomenology, Etiology, Assessment, and Interventions." In Comprehensive Guide to Autism, 601–23. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-4788-7_31.

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Yap, Ivan K. S., and François-Pierre Martin. "Deciphering the Gut Microbial Contribution to the Etiology of Autism Development." In Molecular and Integrative Toxicology, 311–22. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6539-2_14.

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Mazefsky, Carla A., and John Herrington. "Autism and Anxiety: Etiologic Factors and Transdiagnostic Processes." In Handbook of Autism and Anxiety, 91–103. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-06796-4_7.

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Sauer, Ann Katrin, Janelle E. Stanton, Sakshi Hans, and Andreas M. Grabrucker. "Autism Spectrum Disorders: Etiology and Pathology." In Autism Spectrum Disorders, 1–16. Exon Publications, 2021. http://dx.doi.org/10.36255/exonpublications.autismspectrumdisorders.2021.etiology.

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Bhushan Gupta, Vidya. "Etiology of Autism." In Autistic Spectrum Disorders in Children, 42–65. CRC Press, 2004. http://dx.doi.org/10.1201/9780203026229.ch3.

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Conference papers on the topic "Autism – Etiology"

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PENDERGRASS, SARAH, SANTHOSH GIRIRAJAN, and SCOTT SELLECK. "UNCOVERING THE ETIOLOGY OF AUTISM SPECTRUM DISORDERS: GENOMICS, BIOINFORMATICS, ENVIRONMENT, DATA COLLECTION AND EXPLORATION, AND FUTURE POSSIBILITIES." In Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 2013. http://dx.doi.org/10.1142/9789814583220_0041.

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Albuquerque, Julia Berzoini, Débora Rodrigues Martins, Otávio Cosendey Martins, Vívian Maria De Oliveira Gomes, and Francis Moreira Borges. "TRANSTORNO DO ESPECTRO AUTISTA E ALTERAÇÃO DA MICROBIOTA INTESTINAL Autores Julia Berzoini Albuquerque." In I Congresso Nacional de Microbiologia Clínica On-Line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1170.

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Introdução: O Transtorno do Espectro Autista (TEA) é um transtorno de neurodesenvolvimento caracterizado por padrões repetitivos de comportamento e déficits na comunicação e interação social presentes desde a infância. Sua etiologia permanece inconclusiva, mas há indícios de influência genética e de fatores ambientais. Nesse contexto, o eixo microbiota-intestino-cérebro apresenta papel importante, pois sintomas gastrintestinais ocorrem em cerca de 40-60% dos pacientes com TEA e alterações na microbiota podem prejudicar o desenvolvimento. Objetivos: Analisar a relação entre a disbiose intestinal e o Transtorno do Espectro Austista. Material e Métodos: Foi realizada uma revisão bibliográfica narrativa através de busca eletrônica de artigos publicados entre 2017 e 2021, nas bases de dados PubMed e SciElo, sendo os descritores e operadores boleanos “Dysbiosis AND Autism Spectrum Disorder” e “Microbiota AND Autism Spectrum Disorder”. Foram contabilizados 359 artigos, e após triagem dos títulos e resumos, 10 trabalhos foram selecionados. Resultados: Observou-se, quanto às bactérias, aumento da razão Firmicutes/Bacteroidetes, com significativa redução de Bacteroidetes e elevação nos níveis dos gêneros Collinsella e Desulfovibrio. Em relação aos fungos, a proporção de leveduras do gênero Candida em crianças com TEA é duas vezes maior que nas crianças com desenvolvimento típico e anticorpos anti- Candida albicans foram mais encontrados no plasma de crianças com TEA (36,5%) do que no do grupo controle (14,3%). Para as amostras fecais, constatou-se: maior presença de Lactobacillus spp. (68,8%) no grupo controle em relação ao grupo com TEA (27,7%); presença de leucócitos (14,9%) e leveduras (40,4%) no grupo com autismo e ausência destes no grupo controle; e abundância de Clostridium perfringens entre autistas (64,9%) em comparação aos neurotípicos (19,4%). Conclusão: Embora a relação entre a disbiose e o TEA seja descrita na literatura, alguns tópicos ainda permanecem em aberto, como a interferência de tratamentos com antimicrobianos, probióticos e transplante de microbiota fecal na melhora comportamental e o papel da microbiota fúngica nessas condições.
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Lima, Maria Paula Oliveira, and Luiz Fernando Moraes Silva. "ALTERAÇÕES EM REGIÕES NÃO-CODIFICADORAS DO GENOMA NO TRANSTORNO DO ESPECTRO AUTISTA." In II Congresso Brasileiro de Biologia Molecular On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/2316.

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Introdução: O Transtorno do Espectro Autista (TEA) é definido como um transtorno do neurodesenvolvimento caracterizado por dificuldades de comunicação e interação social com padrões repetitivos e estereotipados de comportamento, sendo classificado como “espectro” porque concebe diferentes graus de gravidade. Sua etiologia ainda é desconhecida, mas existem indícios que variações genéticas diversas e fatores ambientais podem afetar o desenvolvimento do cérebro nesta condição. Mutações em regiões que regulam a expressão gênica no DNA codificante de proteínas (éxons) aumentam o risco de desenvolver autismo, e, recentemente foi descoberto que mutações em regiões do DNA não-codificante, antes referidas como “DNA lixo" por serem consideradas não funcionais, podem estar relacionadas ao desenvolvimento do transtorno. Objetivo: Analisar a associação entre mutações em regiões não-codificadoras do DNA com o Transtorno do Espectro Autista. Material e métodos: Foi realizada uma pesquisa bibliográfica nas bases de dados do Google Scholar e PubMed. Foram revisados 10 artigos científicos, utilizando os descritores “Autismo” e “DNA não-codificante” escritos em Inglês e português, publicados de 2015 a 2021. Resultados: Cada indivíduo com autismo pode possuir diferentes variações em sua estrutura genômica. Cerca de 98% do genoma consiste em regiões não-codificantes, que incluem íntrons, regiões promotoras, regiões regulatórias, regiões não traduzíveis (UTRs) e outras que ainda precisam ser exploradas, devido sua amplitude. Em um estudo publicado pela revista Science, conduzido por Sebat, no qual o progresso está sendo baseado em estatísticas do sequenciamento do genoma completo realizado em famílias de indivíduos com TEA, os pesquisadores estavam interessados em partes do DNA não-codificante que regulam a expressão gênica. Foram identificados em indivíduos no espectro autista variantes estruturais nessas regiões, onde grandes sequências de DNA estavam invertidas, duplicadas ou deletadas, quando comparadas com a de seus familiares. Esse estudo também sugere que essas mutações genéticas em indivíduos autistas podem ter sido herdadas de seus pais. Conclusão: Variações genéticas funcionais e regulatórias que ocorrem nas extensas regiões de DNA não-codificante de proteínas ainda permanecem mal compreendidas, necessitando de mais pesquisas que busquem compreender melhor as funções desse tipo de DNA, para que seja possível evidenciar se existe essa associação com desenvolvimento do Transtorno do Espectro Autista.
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Santos, Janine Bruna Rodrigues, and Jessica Adrielle Rodrigues Santos. "FATORES GENÉTICOS RELACIONADOS AO TRANSTORNO DO ESPECTRO AUTISTA (TEA)." In I Congresso Nacional On-line de Biologia Celular e Estrutural. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1945.

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Introdução: O transtorno do espectro autista (TEA) é denominado como um transtorno do neurodesenvolvimento, uma patologia psiquiátrica caracterizada por déficit de comunicação, dificuldade de interação social e comportamental. Sua etiologia ainda não é totalmente conhecida, porém acredita-se que fatores genéticos estão fortemente ligados ao desenvolvimento da doença o que se tornou intenso objeto de estudo entre os muitos pesquisadores. Objetivo: Realizar uma revisão bibliográfica sobre os fatores genéticos relacionados ao Transtornos do Espectro autista. Materiais e Métodos: Constitui uma revisão bibliográfica de caráter analítico e comparativo a respeito dos fatores genéticos relacionados ao surgimento do Transtorno do Espectro Autista (TEA). Resultados: O TEA é um transtorno psiquiátrico em geral diagnosticado clinicamente na infância. Seus primeiros sinais aparecem ainda na fase de lactentes com dificuldades de socialização e afetivas bem como presença de deficiências no aprendizado. Embora fatores ambientais como os poluentes ou outras razões como o uso de medicações ou as infecções durante a gravidez possam estar ligados ao aparecimento do transtorno do espectro autista, estima-se que a patogênese da doença esteja relacionada à genética. Estudos recentes, graças ao uso de novas tecnologias atreladas ao estudos de genes, apontam uma herdabilidade de aproximadamente 90% dos casos de TEA. Isso reforça a necessidade da continuidade sobre pesquisas e mapeamento dos genes do Transtorno do espectro autista que permite, não só conhecer a etiologia da doença, mas também verificar as comorbidades associadas a ela além de, possivelmente descobrir formas de diagnósticos e possibilidades de tratamentos personalizados para melhoria da qualidade de vida dos pacientes. Conclusão: Dessa maneira, é de extrema necessidade, o investimento de estudos em mapeamento genético, além de orientar os familiares de pacientes quanto ao aconselhamento genético, a fim de promover maior conhecimento acerca da etiologia do TEA, com o intuito de proporcionar melhoria na qualidade de vida das crianças portadoras da doença reduzindo sintomas indesejáveis e desfechos negativos do transtornos do espectro autista.
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Reports on the topic "Autism – Etiology"

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Mong, Jessica. Etiology of Sleep Disorders in ASD (Autism Spectrum Disorders): Role for Inflammatory Cytokines. Fort Belvoir, VA: Defense Technical Information Center, May 2011. http://dx.doi.org/10.21236/ada581407.

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Liu, Xudong. MTHFR Functional Polymorphism C677T and Genomic Instability in the Etiology of Idiopathic Autism in Simplex Families. Revision. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada600503.

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