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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Currenti, Salvatore A. "Understanding and Determining the Etiology of Autism." Cellular and Molecular Neurobiology 30, no. 2 (September 23, 2009): 161–71. http://dx.doi.org/10.1007/s10571-009-9453-8.

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12

Lavrov, Nikanor V., and Petr D. Shabanov. "Autism spectrum disorders: etiology, treatment. models and experimental studies." Reviews on Clinical Pharmacology and Drug Therapy 16, no. 1 (March 15, 2018): 21–27. http://dx.doi.org/10.17816/rcf16121-27.

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The study of disorders of brain activity related to the violation of socialization is the current scientific problem. The article presents a review of the literature regarding the epidemiology, etiology and treatment of autism spectrum disorders. Special attention is paid to experimental models of autism, since simulation allows to test hypotheses about the nature of the disease and to carry out testing of new treatment methods. (For citation: Lavrov NV, Shabanov PD. Autism spectrum disorders: etiology, treatment. Models and experimental studies. Reviews on Clinical Pharmacology and Drug Therapy. 2018;16(1):21-27. doi: 10.17816/RCF16121-27).
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13

Finucane, Brenda, Barbara Haas-Givler, and Elliott W. Simon. "Knowledge and Perceptions About Fragile X Syndrome: Implications for Diagnosis, Intervention, and Research." Intellectual and Developmental Disabilities 51, no. 4 (August 1, 2013): 226–36. http://dx.doi.org/10.1352/1934-9556-51.4.226.

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Abstract We surveyed 439 professionals in the field of autism to assess their knowledge and perceptions about fragile X syndrome (FXS) and related issues. Almost half had worked with at least one child diagnosed with FXS, yet most lacked basic knowledge about the condition, underestimated its significance in the etiology of autism spectrum disorders, and rarely accessed fragile X–specific resources. A majority perceived etiology to be an important variable in therapeutic response while three quarters felt that professionals in the field of autism should play an active role in referring children for etiological evaluation. Despite these opinions, most respondents either rarely or never inquired about etiology when working with a new client. The survey results underscore the need for training and education so that autism professionals can become effective partners in diagnostic genetic referral and in research and implementation of syndrome-specific interventions.
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14

Varvara, Tsopanidou, and Athanasios Drigas. "Environmental factors and their effect on the occurrence of autism." Technium BioChemMed 3, no. 1 (February 28, 2022): 34–41. http://dx.doi.org/10.47577/biochemmed.v3i1.5877.

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The etiology of autism is the subject of intense research. Genetic factors are clearly important. Gene mutations, gene deletions, copy number variations (CNVs) and other genetic abnormalities are strongly linked to autism. But no etiology represents more than a relatively small percentage of cases. Environmental factors in recent years are increasingly coming to the forefront of research and study and the interest of researchers is increasingly directed in this direction. This article examines the environmental factors associated with the prenatal period and their relationship to autism.
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15

Bertone, Armando, Laurent Mottron, and Jocelyn Faubert. "Autism and schizophrenia: Similar perceptual consequence, different neurobiological etiology?" Behavioral and Brain Sciences 27, no. 4 (August 2004): 592–93. http://dx.doi.org/10.1017/s0140525x04260137.

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Phillips & Silverstein (P&S, 2003) propose that NMDA-receptor dysfunction may be the fundamental neurobiological mechanism underlying and associating impaired holistic perception and cognitive coordination with schizophrenic psychopathology. We discuss how the P&S hypothesis shares different aspects of the weak central coherence account of autism from both theoretical and experimental perspectives. Specifically, we believe that neither those persons with autism nor those with schizophrenia integrate visuo-perceptual information efficiently, resulting in incongruous internal representations of their external world. However, although NMDA-hypofunction may be responsible for perceptual impairments in schizophrenia and possibly autism, we suggest that it is highly unlikely that NMDA-hypofunction is specifically responsible for the autistic behavioral symptomology, as described by P&S in their target article.
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16

Yoon, Sang Hoon, Joonhyuk Choi, Won Ji Lee, and Jeong Tae Do. "Genetic and Epigenetic Etiology Underlying Autism Spectrum Disorder." Journal of Clinical Medicine 9, no. 4 (March 31, 2020): 966. http://dx.doi.org/10.3390/jcm9040966.

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Autism spectrum disorder (ASD) is a pervasive neurodevelopmental disorder characterized by difficulties in social interaction, language development delays, repeated body movements, and markedly deteriorated activities and interests. Environmental factors, such as viral infection, parental age, and zinc deficiency, can be plausible contributors to ASD susceptibility. As ASD is highly heritable, genetic risk factors involved in neurodevelopment, neural communication, and social interaction provide important clues in explaining the etiology of ASD. Accumulated evidence also shows an important role of epigenetic factors, such as DNA methylation, histone modification, and noncoding RNA, in ASD etiology. In this review, we compiled the research published to date and described the genetic and epigenetic epidemiology together with environmental risk factors underlying the etiology of the different phenotypes of ASD.
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17

Tsipan, R. M., C. I. Parenteau, and R. L. Hendren. "Integrating Treatment for Autism: Etiology and Life Cycle." Autism and Developmental Disorders 18, no. 3 (2020): 28–37. http://dx.doi.org/10.17759/autdd.2020180304.

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Autism Spectrum Disorder (ASD) is linked to a multitude of genes, epigenetics, and environmental factors, which contribute to the complexities of treating ASD. A large body of literature suggests benefits from perinatal, early, and later intervention. It is common for physicians to struggle with making a diagnosis of ASD, but once it is made, parents who have been taught effective strategies can be impactful in their child’s positive development. Neuroimaging studies of children, adolescents and young adults with ASD suggest that their brain structures change over time and are also capable of being shaped through appropriate interventions. Interventions are also being adapted for adults with ASD to better address their needs, such as employment training programs. We review the wide array of risk factors and interventions to mitigate the challenges individuals with ASD face in their daily lives.
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18

Mano, Elona. "ETIOLOGY OF AUTISM AND PARENTS OF AUTISTIC CHILDREN." IJASOS- International E-journal of Advances in Social Sciences 2, no. 4 (2016): 283. http://dx.doi.org/10.18769/ijasos.69079.

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19

Correia, F., C. Café, J. Almeida, S. Mouga, and G. Oliveira. "Autism Spectrum Disorder: FRAXE Mutation, a Rare Etiology." Journal of Autism and Developmental Disorders 45, no. 3 (July 18, 2014): 888–92. http://dx.doi.org/10.1007/s10803-014-2185-8.

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20

Phelps, LeAdelle, and Jo Anne Grabowski. "Autism: Etiology, differential diagnosis, and behavioral assessment update." Journal of Psychopathology and Behavioral Assessment 13, no. 2 (June 1991): 107–25. http://dx.doi.org/10.1007/bf00961426.

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21

Maksimović, Nataša, and Darija Kisić-Tepavčević. "Autism and MMR vaccine." Medicinska istrazivanja 52, no. 3 (2018): 14–19. http://dx.doi.org/10.5937/medist1801014m.

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Autism is a complex neurological developmental disorder with wide range of symptoms. Among them, poor social interaction, limited and repeated behavioral patterns are the most important for diagnosing the disorder. The prevalence of autism is rising constantly. One of the theories drawing the greatest public attention for a long time is a possible association between MMR vaccine and risk of autism. The first study aimed to investigate this association is the one conducted in 1998. As the results supported the theory that MMR vaccine increased the risk of autism, MMR immunization coverage decreased dramatically which further led to measles outbreaks, even in those countries where the disease was almost eradicated. Soon after that publication, new studies denying any association between MMR vaccine and risk of autism were published. Among them, systematic review published in 2012, including 57 epidemiological studies with 14.700.000 children is particularly important. Although the etiology of autism is not completely clarified, there are strong evidence on the presence of neurobiological changes with significant genetic component underlying the etiology. According to recent literature data, morphological changes in brain of children age 6 to 12 months, that is, before the administration of MMR vaccine, precede clinical symptoms of autism.
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22

El Hazmi, M. A. "Autism and mental retardation: the genetic relationship and contribution." Eastern Mediterranean Health Journal 7, no. 3 (September 15, 2001): 536–43. http://dx.doi.org/10.26719/2001.7.3.536.

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Autism, a neurodevelopmental disorder first described in 1943, is reviewed. The signs and symptoms of the disorder are described together with the etiological factors. The evidence for a genetic etiology of autism and its association with other genetic disorders are discussed. Possible candidate genes for autism are described.
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23

SMITH, SHELLEY D., and COLLEEN A. MORRIS. "Planning studies of etiology." Applied Psycholinguistics 26, no. 1 (January 2005): 97–110. http://dx.doi.org/10.1017/s0142716405050083.

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Knowledge of the environmental and genetic etiologies of complex cognitive disorders can guide strategies for diagnosis, prevention, and therapy, but disentangling the various causes can be very challenging. Two basic approaches can be used in identifying genetic factors, a top-down approach, in which phenotypic descriptions are used to discover genes that influence those phenotypes, and a bottom-up approach, comparing the phenotypic effects of genes that are known to cause syndromes that include cognitive disabilities. Thorough characterization of phenotypes throughout development is critical to both of these methods. These strategies have been applied to the characterization of genetic etiologies for reading disability, language disorders, attention-deficit hyperactivity disorder, and autism.
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24

Gerdts, Jennifer, and Raphael Bernier. "The Broader Autism Phenotype and Its Implications on the Etiology and Treatment of Autism Spectrum Disorders." Autism Research and Treatment 2011 (2011): 1–19. http://dx.doi.org/10.1155/2011/545901.

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The presence of autism-related traits has been well documented in undiagnosed family members of individuals with autism spectrum disorder (ASD). The most common finding is mild impairments in social and communication skills that are similar to those shown by individuals with autism, but exhibited to a lesser degree. Termed thebroader autism phenotype(BAP), these traits suggest a genetic liability for autism-related traits in families. Genetic influence in autism is strong, with identical twins showing high concordance for the diagnosis and related traits and approximately 20% of all ASD cases having an identified genetic mechanism. This paper highlights the studies conducted to date regarding the BAP and considers the implications of these findings for the etiology and treatment of ASD.
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25

Rubenstein, Eric, Lisa D. Wiggins, Laura A. Schieve, Chyrise Bradley, Carolyn DiGuiseppi, Eric Moody, Juhi Pandey, et al. "Associations between parental broader autism phenotype and child autism spectrum disorder phenotype in the Study to Explore Early Development." Autism 23, no. 2 (January 29, 2018): 436–48. http://dx.doi.org/10.1177/1362361317753563.

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The autism spectrum disorder phenotype varies by social and communication ability and co-occurring developmental, behavioral, and medical conditions. Etiology is also diverse, with myriad potential genetic origins and environmental risk factors. Examining the influence of parental broader autism phenotype—a set of sub-clinical characteristics of autism spectrum disorder—on child autism spectrum disorder phenotypes may help reduce heterogeneity in potential genetic predisposition for autism spectrum disorder. We assessed the associations between parental broader autism phenotype and child phenotype among children of age 30–68 months enrolled in the Study to Explore Early Development (N = 707). Child autism spectrum disorder phenotype was defined by a replication of latent classes derived from multiple developmental and behavioral measures: Mild Language Delay with Cognitive Rigidity, Mild Language and Motor Delay with Dysregulation (e.g. anxiety/depression), General Developmental Delay, and Significant Developmental Delay with Repetitive Motor Behaviors. Scores on the Social Responsiveness Scale-Adult measured parent broader autism phenotype. Broader autism phenotype in at least one parent was associated with a child having increased odds of being classified as mild language and motor delay with dysregulation compared to significant developmental delay with repetitive motor behaviors (odds ratio: 2.44; 95% confidence interval: 1.16, 5.09). Children of parents with broader autism phenotype were more likely to have a phenotype qualitatively similar to broader autism phenotype presentation; this may have implications for etiologic research.
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Packer, Alan. "Neocortical neurogenesis and the etiology of autism spectrum disorder." Neuroscience & Biobehavioral Reviews 64 (May 2016): 185–95. http://dx.doi.org/10.1016/j.neubiorev.2016.03.002.

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27

Steinman, Gary, and David Mankuta. "Insulin-like growth factor and the etiology of autism." Medical Hypotheses 80, no. 4 (April 2013): 475–80. http://dx.doi.org/10.1016/j.mehy.2013.01.010.

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28

Arehart-Treichel, Joan. "Which Weighs More in Autism Etiology: Genes or Environment?" Psychiatric News 46, no. 16 (August 19, 2011): 16. http://dx.doi.org/10.1176/pn.46.16.psychnews_46_16_16_2.

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29

Chen, Donna T., Franklin G. Miller, and Donald L. Rosenstein. "Ethical aspects of research into the etiology of autism." Mental Retardation and Developmental Disabilities Research Reviews 9, no. 1 (2003): 48–53. http://dx.doi.org/10.1002/mrdd.10059.

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30

袁, 瑞婕. "New Progress in the Etiology and Treatment of Autism." Advances in Psychology 10, no. 05 (2020): 580–88. http://dx.doi.org/10.12677/ap.2020.105072.

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31

PIVEN, JOSEPH, JON SIMON, GARY A. CHASE, MARYANN WZOREK, REBECCA LANDA, JEANNE GAYLE, and SUSAN FOLSTEIN. "The Etiology of Autism: Pre-, Peri- and Neonatal Factors." Journal of the American Academy of Child & Adolescent Psychiatry 32, no. 6 (November 1993): 1256–63. http://dx.doi.org/10.1097/00004583-199311000-00021.

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32

Moran, Mark. "With Vaccine Theory Discredited, Hunt for Autism Etiology Continues." Psychiatric News 39, no. 13 (July 2, 2004): 44. http://dx.doi.org/10.1176/pn.39.13.0390044.

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33

Orefice, Lauren L. "Outside-in: Rethinking the etiology of autism spectrum disorders." Science 366, no. 6461 (October 3, 2019): 45–46. http://dx.doi.org/10.1126/science.aaz3880.

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34

Hassan, Mariam M., and Hoda M. O. Mokhtar. "Investigating autism etiology and heterogeneity by decision tree algorithm." Informatics in Medicine Unlocked 16 (2019): 100215. http://dx.doi.org/10.1016/j.imu.2019.100215.

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35

Malow, Beth, and Angela Maxwell-Horn. "Sleep in Autism." Seminars in Neurology 37, no. 04 (August 2017): 413–18. http://dx.doi.org/10.1055/s-0037-1604353.

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AbstractAutism spectrum disorder (ASD) is a neurodevelopmental disorder that has increased in prevalence over the last several decades. A significant proportion of children with ASD have comorbid sleep disorders. The interplay between ASD and sleep is multifactorial and bidirectional. There is evidence for physiological differences in ASD that contribute to sleep problems, including sensory overresponsiveness (SOR) and abnormal melatonin production. Comorbidities associated with ASD (attention deficit hyperactivity disorder [ADHD], mood disorders) as well as medications used to treat these comorbidities often have effects on sleep architecture. In this article the authors discuss the etiology and manifestations of sleep disorders in children with ASD, as well as their clinical evaluation and treatment options.
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36

Płatos, Mateusz. "Autyzm odcieleśniony. Historia społecznego konstruowania autyzmu… jako choroby, zaburzenia i niepełnosprawności." Annales Universitatis Paedagogicae Cracoviensis. Studia de Cultura, no. 10(1) (March 2018): 100–112. http://dx.doi.org/10.24917/20837275.10.1.8.

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Autism disembodied. The history of social construction of autism as illness, disorder, and disability The article is an attempt to look at the history of discourse about autism from the perspective of autism studies. Due to the blurred definition and yet unknown etiology autism was used as a space for modern cultural projections about disability and mental illness. As I argue, both the determination of modern scientific institutions and their failure to objectify autism using empirical methods are linked to the disembodied nature of autism, which still reveals it arbitrariness and social – not natural – construction. As late as in 21th century, autistic people have joined the discourse about themselves, trying to make autism a positive and integral aspect of their identity. Keywords: autism, Asperger syndrome, disability, mental illness, eugenics
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37

Tager-Flusberg, Helen, and Robert M. Joseph. "Identifying neurocognitive phenotypes in autism." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 358, no. 1430 (February 28, 2003): 303–14. http://dx.doi.org/10.1098/rstb.2002.1198.

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Autism is a complex disorder that is heterogeneous both in its phenotypic expression and its etiology. The search for genes associated with autism and the neurobiological mechanisms that underlie its behavioural symptoms has been hampered by this heterogeneity. Recent studies indicate that within autism, there may be distinct subgroups that can be defined based on differences in neurocognitive profiles. This paper presents evidence for two kinds of subtypes in autism that are defined on the basis of language profiles and on the basis of cognitive profiles. The implications for genetic and neurobiological studies of these subgroups are discussed, with special reference to evidence relating these cognitive phenotypes to volumetric studies of brain size and organization in autism.
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Ustinova, Nataliya V., and Leyla S. Namazova-Baranova. "Role of Pediatrician in Early Risk Evaluation, Diagnosis and Management of Children with Autism Spectrum Disorders." Current Pediatrics 20, no. 2 (May 18, 2021): 116–21. http://dx.doi.org/10.15690/vsp.v20i2.2255.

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The article discusses recent ideas about autism: classification approaches, incidence, etiology and pathogenesis, clinical manifestations and diagnosis, comorbid medical conditions, early detection approaches and medical care for children with autism spectrum disorders. The focus is on the information needed for pediatricians in their practice to provide effective medical care for children with neurodevelopmental disorders.
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39

Derguy, C., M. Bouvard, G. Michel, and K. M’Bailara. "The gap between parents’ knowledge and causal beliefs about etiology of autism: A key variable to understand parents’ anxiety." European Psychiatry 29, S3 (November 2014): 598–99. http://dx.doi.org/10.1016/j.eurpsy.2014.09.195.

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Autism Spectrum Disorders (ASD) are associated with higher levels of anxiety for parents [1]. Provide medical information about autism etiology is the first step to help parents to understand the child disorder and to cope with it. The medical current community accepts that autism is a neurodevelopmental disorder in which genes play a role but that environmental factors likely contribute as well [2]. This conception can meet parent's beliefs constructed on their cultural values and personal experiences. In line with causal attribution theory [3], it is important to consider to parental beliefs because it can impact the treatment choices and the child developmental trajectory [4]. The Main purpose is to evaluate the consistency between parental knowledge and beliefs about ASD etiology. The second purpose is to explore the impact of consistency on parents’ anxiety. We interviewed through open-ended questions 89 parents of ASD children aged between 3 to 10 years about their knowledge and their beliefs about ASD etiology. A content analysis was performed using the Nvivo10 software. Anxiety is evaluated with the subscale of the Hospital Anxiety and Depression Scale (HADS). In agreement with previous work four categories of causes have been identified: biological (BIO), psychological (PSY), multifactorial etiology (BIO + PSY), others (OT). A percentage of 55.1% of parents is consistent between their knowledge and beliefs about ASD etiology while 43.8% are inconsistent. Parent anxiety is significantly higher (T (71.91) = 2.34; P < 0.05) when knowledge and beliefs are inconsistent than when they are consistent. This study demonstrates the deleterious impact of inconsistency between knowledge and beliefs about ASD etiology, on parental anxiety. In order to provide relevant support for parents, information delivered after diagnosis must consider pre-existing parental beliefs. A systematic assessment of parental beliefs would adjust the information provided after the diagnosis.
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40

Greenberg, David A., Susan E. Hodge, Janice Sowinski, and Doug Nicoll. "Excess of Twins among Affected Sibling Pairs with Autism: Implications for the Etiology of Autism." American Journal of Human Genetics 69, no. 5 (November 2001): 1062–67. http://dx.doi.org/10.1086/324191.

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41

Kim, Bora, Mina Ha, Young Shin Kim, Yun-Joo Koh, Shan Dong, Ho-Jang Kwon, Young-Suk Kim, et al. "Prenatal exposure to paternal smoking and likelihood for autism spectrum disorder." Autism 25, no. 7 (April 20, 2021): 1946–59. http://dx.doi.org/10.1177/13623613211007319.

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Genetics, environment, and their interactions impact autism spectrum disorder etiology. Smoking is a suspected autism spectrum disorder risk factor due to biological plausibility and high prevalence. Using two large epidemiological samples, we examined whether autism spectrum disorder was associated with prenatal paternal smoking in a Discovery sample ( N = 10,245) and an independent Replication sample ( N = 29,773). Paternal smoking was retrospectively assessed with questionnaires. Likelihood of having autism spectrum disorder was estimated with the Autism Spectrum Screening Questionnaire at three levels: low (<10), intermediate (10–14), and high (⩾15). Ordinal regression was used to examine the relationship between prenatal paternal smoking and likelihood of having autism spectrum disorder, adjusting for confounders. A total of 36.5% of Discovery sample fathers and 63.3% of Replication sample fathers smoked during the pregnancy period; 7% of the Replication sample smoker fathers smoked during the pre-conception period but quit during pregnancy period. Discovery sample prenatal paternal smoking significantly increased the likelihood of having autism spectrum disorder in their offspring (adjusted odds ratio=1.27). This was confirmed in the Replication sample with adjusted odds ratio of 1.15 among smoking pre-conception period + pregnancy period fathers; 14.4% and 11.1% increased high likelihood of autism spectrum disorder was attributable to prenatal paternal smoking in Discovery sample and Replication sample, respectively. Smoking prevention, especially in pregnancy planning, may decrease autism spectrum disorder risk in offspring. Lay abstract What is Already Known about This Subject: Genetics, (including de novo mutations), environmental factors (including toxic exposures), and their interactions impact autism spectrum disorder etiology. Paternal smoking is a candidate risk for autism spectrum disorder due to biological plausibility, high prevalence, and potential intervention. What This Study Adds: This original study and its replication confirms that paternal factors can substantially contribute to autism spectrum disorder risk for their offspring. It specifically indicates that paternal smoking both before and during pregnancy contributes significantly to autism spectrum disorder risk. Implications for practice, research, or policy: Smoking prevention, especially in pregnancy planning, may decrease autism spectrum disorder risk in offspring.
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42

Hollander, Eric, Charles Cartwright, Cheryl M. Wong, Concetta M. DeCaria, Gina DelGiudice-Asch, Monte S. Buchsbaum, and Bonnie R. Aronowitz. "A Dimensional Approach to the Autism Spectrum." CNS Spectrums 3, no. 3 (March 1998): 22–39. http://dx.doi.org/10.1017/s1092852900005678.

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AbstractAutism is heterogeneous with respect to clinical symptoms and etiology. A significant limitation in research of the neurobiology and treatment of autism has been the lack of attention to this heterogeneity. A dimensional approach to the study of autism is valuable in linking key symptoms to the neurobiology and treatment of the disorder in a clinically meaningful way. In this article, we outline a dimensional approach to the autism spectrum, discuss the three core dimensions of autism and their neurobiology, and review the possible links of serotonin, anterior cingulate gyrus activity, and the immune marker D8/17 to the repetitive behavior/compulsivity dimensions.
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43

Goel, Aanya, and Michael Aschner. "The Effect of Lead Exposure on Autism Development." International Journal of Molecular Sciences 22, no. 4 (February 6, 2021): 1637. http://dx.doi.org/10.3390/ijms22041637.

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Autism Spectrum Disorder (ASD) remains one of the most detrimental neurodevelopmental conditions in society today. Common symptoms include diminished social and communication ability. Investigations on autism etiology remain largely ambiguous. Previous studies have highlighted exposure to lead (Pb) may play a role in ASD. In addition, lead has been shown to be one of the most prevalent metal exposures associated with neurological deficits. A semi-systematic review was conducted using public databases in order to evaluate the extent of lead’s role in the etiology of autism. This review examines the relationship between autistic comorbid symptoms—such as deterioration in intelligence scores, memory, language ability, and social interaction—and lead exposure. Specifically, the mechanisms of action of lead exposure, including changes within the cholinergic, dopaminergic, glutamatergic, gamma aminobutyric acid (GABA)ergic systems, are discussed. The goal of this review is to help illustrate the connections between lead’s mechanistic interference and the possible furthering of the comorbidities of ASD. Considerations of the current data and trends suggest a potential strong role for lead in ASD.
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44

Matson, Johnny L., Alison M. Kozlowski, and Michael M. Matson. "Speech deficits in persons with autism: Etiology and symptom presentation." Research in Autism Spectrum Disorders 6, no. 2 (April 2012): 573–77. http://dx.doi.org/10.1016/j.rasd.2011.10.009.

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45

Fatemi, S. Hossein. "The Role of Neurodevelopmental Genes in Infectious Etiology of Autism." American Journal of Biochemistry and Biotechnology 4, no. 2 (February 1, 2008): 177–82. http://dx.doi.org/10.3844/ajbbsp.2008.177.182.

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Patterson, Paul. "IMMUNE INVOLVEMENT IN AUTISM & SCHIZOPHRENIA: ETIOLOGY AND AN ANIMALMODEL." Schizophrenia Research 102, no. 1-3 (June 2008): 31. http://dx.doi.org/10.1016/s0920-9964(08)70097-5.

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Risch, Neil, Donna Spiker, Linda Lotspeich, Nassim Nouri, David Hinds, Joachim Hallmayer, Luba Kalaydjieva, et al. "A Genomic Screen of Autism: Evidence for a Multilocus Etiology." American Journal of Human Genetics 65, no. 2 (August 1999): 493–507. http://dx.doi.org/10.1086/302497.

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48

Steinman, Gary. "Plausible etiology of brain dysconnectivity in autism – Review and prospectus." Medical Hypotheses 85, no. 4 (October 2015): 405–7. http://dx.doi.org/10.1016/j.mehy.2015.06.018.

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49

Fluegge, Keith. "Methyl B12 and Autism Spectrum Disorders: Any Clues to Etiology?" Journal of Child and Adolescent Psychopharmacology 26, no. 9 (November 2016): 853. http://dx.doi.org/10.1089/cap.2016.0038.

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50

Ruthsatz, Joanne, Stephen A. Petrill, Ning Li, Samuel L. Wolock, and Christopher W. Bartlett. "Molecular Genetic Evidence for Shared Etiology of Autism and Prodigy." Human Heredity 79, no. 2 (2015): 53–59. http://dx.doi.org/10.1159/000373890.

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