Autism in Thalidomide Embryopathy: A Population Study

Strömland, Kerstin; Nordin, Viviann; Miller, Marilyn T.; Åkerström, Bengt; Gillberg, Christopher

doi:10.1111/j.1469-8749.1994.tb11856.x

Cited by 392 publications

(169 citation statements)

References 11 publications

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“…As noted previously, autism risk factors include environmental challenges, such as maternal use of pharmaceutical agents with neurotoxic effects, [226][227][228]241,242 prenatal exposure to viral infections or maternal stress 233,234 and, in addition, exposure to high levels of environmental pollutants, including heavy metals. 275,276 A recent review by Herbert et al 7 identified 135 genes that have been shown to mediate responses to environmental challenge, and that are located within autism linkage regions.…”

Section: Genes Responsive To Environmental Factorsmentioning

confidence: 97%

“…[235][236][237] These physical manifestations are predictive of greater symptom severity and neuroanatomical abnormalities. 235,238,239 Exposure to teratogens during gestation has also been shown to be a risk factor for autism, with higher disease incidence associated with maternal use of valproic acid, [226][227][228]240 thalidomide 241 and misoprostol. 242 The detrimental neurodevelopmental effects of maternal infection have been attributed, in part, to the induction of inflammatory cytokines.…”

Section: Mouse Models Of Environmental Contributions To Autism Etiologymentioning

confidence: 99%

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Advances in behavioral genetics: mouse models of autism

2007

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Autism is a neurodevelopmental syndrome with markedly high heritability. The diagnostic indicators of autism are core behavioral symptoms, rather than definitive neuropathological markers. Etiology is thought to involve complex, multigenic interactions and possible environmental contributions. In this review, we focus on genetic pathways with multiple members represented in autism candidate gene lists. Many of these pathways can also be impinged upon by environmental risk factors associated with the disorder. The mouse model system provides a method to experimentally manipulate candidate genes for autism susceptibility, and to use environmental challenges to drive aberrant gene expression and cell pathology early in development. Mouse models for fragile X syndrome, Rett syndrome and other disorders associated with autistic-like behavior have elucidated neuropathology that might underlie the autism phenotype, including abnormalities in synaptic plasticity. Mouse models have also been used to investigate the effects of alterations in signaling pathways on neuronal migration, neurotransmission and brain anatomy, relevant to findings in autistic populations. Advances have included the evaluation of mouse models with behavioral assays designed to reflect disease symptoms, including impaired social interaction, communication deficits and repetitive behaviors, and the symptom onset during the neonatal period. Research focusing on the effect of gene-by-gene interactions or genetic susceptibility to detrimental environmental challenges may further understanding of the complex etiology for autism.

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Section: Genes Responsive To Environmental Factorsmentioning

confidence: 97%

Section: Mouse Models Of Environmental Contributions To Autism Etiologymentioning

confidence: 99%

Advances in behavioral genetics: mouse models of autism

2007

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“…These agents could directly damage the mitochondria and reduce their efficiency, or impair functional activity by increasing body burden of free radicals and resultant oxidative stress. Drugs like valproic acid and thalidomide [68,69] , as well as exposure to viruses such as rubella and cytomegalovirus [70,71] are examples of environmental factors that have a known causal role in autism. However, many more environmental toxins including pesticides [53,72] , polychlorinated biphenyls (PCB's) [73] , industrial chemicals [73][74][75][76] , and toxic metals such as mercury [77,78] , lead [79,80] , cadmium, nickel [74] , and tin [81] have also been implicated in ASD.…”

Section: Possible Causes Of Mtd In Autismmentioning

confidence: 99%

Evidence of Mitochondrial Dysfunction in Autism and Implications for Treatment

Rossignol¹,

Bradstreet²

2008

American J. of Biochemistry and Biotechnology

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Classical mitochondrial diseases occur in a subset of individuals with autism and are usually caused by genetic anomalies or mitochondrial respiratory pathway deficits. However, in many cases of autism, there is evidence of mitochondrial dysfunction (MtD) without the classic features associated with mitochondrial disease. MtD appears to be more common in autism and presents with less severe signs and symptoms. It is not associated with discernable mitochondrial pathology in muscle biopsy specimens despite objective evidence of lowered mitochondrial functioning. Exposure to environmental toxins is the likely etiology for MtD in autism. This dysfunction then contributes to a number of diagnostic symptoms and comorbidities observed in autism including: cognitive impairment, language deficits, abnormal energy metabolism, chronic gastrointestinal problems, abnormalities in fatty acid oxidation, and increased oxidative stress. MtD and oxidative stress may also explain the high male to female ratio found in autism due to increased male vulnerability to these dysfunctions. Biomarkers for mitochondrial dysfunction have been identified, but seem widely under-utilized despite available therapeutic interventions. Nutritional supplementation to decrease oxidative stress along with factors to improve reduced glutathione, as well as hyperbaric oxygen therapy (HBOT) represent supported and rationale approaches. The underlying pathophysiology and autistic symptoms of affected individuals would be expected to either improve or cease worsening once effective treatment for MtD is implemented.

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“…In Japan, the prevalence of autistic disorders has been reported to be 3 times higher in children hospitalized in neonatal care units than in the general population [28]. In some cases, autism is associated with insults early in gestation, including thalidomide embryopathy in 4% to 5% of cases, probably due to damage to the CNS in the early stages of gestation [29]. Autism occasionally occurs as a result of maternal ingestion of anticonvulsants [30].…”

Section: Pre-and Perinatal Factorsmentioning

confidence: 99%

Autism-A Multifaceted Diffuse Pathology

Brejlova¹,

Domkarova²,

Stefano³

2015

J Psychiatry

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Journal of Psychiatry AbstractThe causes of pervasive developmental disorders have yet to be resolved. Needless to say, the etiology is complex as are the individual factors, especially in regard to autism. Certain findings may be integrated into early coherent models, but the heterogeneity of findings remains a central feature of autism. The present review examines contemporary areas of research and a few prominent theories specifically dealing with autism. The areas under scrutiny are divided into common academic compartments, such as biological, environmental. Autism represents a very timely topic due to its rising incidence in the population as well as changes in previous concepts occurring at this time. Besides the neurological, biological and epidemiological factors contributing and possibly initiating this disorder we discuss the possible involvement of endogenous morphine, especially in regard to depression and limbic functions. Lastly, we advance the theory that dysfunctional mitochondria appear to be involved in autism as well, explaining the widespread occurrence of its characteristics within the construct of susceptibility to stress and trauma. Thus, the diffuse manifestations of Pervasive Developmental Disorder occur potentially by altering energy processes.

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Autism in Thalidomide Embryopathy: A Population Study

Cited by 392 publications

References 11 publications

Advances in behavioral genetics: mouse models of autism

Advances in behavioral genetics: mouse models of autism

Evidence of Mitochondrial Dysfunction in Autism and Implications for Treatment

Autism-A Multifaceted Diffuse Pathology

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