Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004352 (autism)
 32,579 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Testosterone promotes male-typical neural and behavioral development in non-human mammals. There is growing evidence that testosterone exerts similar influences on human development, although the range of behaviors affected is not completely known. This study examined the hypothesis that autistic traits are increased following prenatal exposure to abnormally high levels of testosterone caused by congenital adrenal hyperplasia (CAH). Sixty individuals with CAH (34 female, 26 male) and 49 unaffected relatives (24 female, 25 male) completed the Autism Spectrum Quotient (AQ). Females with CAH scored significantly higher than unaffected females on total AQ score, largely due to enhanced scores on subscales measuring social skills and imagination. These results suggest that prenatal exposure to high levels of testosterone influences some autistic traits and that hormonal factors may be involved in vulnerability to autism.
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PMID:Androgens and autistic traits: A study of individuals with congenital adrenal hyperplasia. 1662 15

Autism spectrum disorders (ASD) are a set of heterogeneous neurodevelopmental conditions, characterized by early-onset difficulties in social communication and unusually restricted, repetitive behavior and interests. Children with ASD have a high rate of irritability and aggressive symptoms which have significant impact on their lives, families and society. The etiology of aggression in humans is likely complex and includes both biological and behavioral causes. Biological approaches have focused on hormones and neurotransmitters that are hypothesized to contribute to the etiology and clinical manifestation of aggressive behavior in humans. Testosterone is a male sex hormone and some studies suggest that it can play a role in the complex etiology of aggressive behavior. Two specific subtypes of aggression have been identified: explosive and non-explosive. Explosive aggression is accompanied by a raged affect and is usually more dangerous and not immediately responsive to behavioral treatment. In our review we would like to provide current findings and discuss potential limitation of research in this area. We propose to determine bio-behavioral model of explosive aggression in children with ASD which will predict which children will be most responsive to potential antiandrogen therapy and behavioral therapy.
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PMID:Testosterone and explosive aggression in autism spectrum disorders. 2561 77

Children with autism spectrum disorders (ASD) have a high rate of irritability and aggressive symptoms which have significant impact on their lives, families and society. The etiology of aggression in humans is likely complex and includes both biological and behavioral causes. Biological approaches have focused on hormones and neurotransmitters that are hypothesized to contribute to the etiology and clinical manifestation of aggressive behavior in humans. Testosterone is a male sex hormone and some studies suggest that it can play a role in the complex etiology of aggressive behavior. Two specific subtypes of aggression have been identified: explosive and non-explosive. Explosive aggression is accompanied by a raged affect and is usually more dangerous and not immediately responsive to behavioral treatment. We propose that individuals with ASD and explosive aggression will have higher androgen activity and higher arousal than neurotypical children and children with ASD without explosive aggression. We employed a unique method for aggression assessment- functional behavioral analysis- to obtain objective and quantitative measures of aggression and arousal signs. In our pilot study, we proposed to determine bio-behavioral model of explosive aggression in children with ASD which will predict which children will be most responsive to antiandrogen therapy and behavioral therapy (Tab. 1, Fig. 1, Ref. 31).
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PMID:Bio-behavioral model of aggression in autism spectrum disorders-pilot study. 2692 48

Valproic acid (VPA) is an anti-epileptic drug with teratogenicity activity that has been related to autism. In rodents, exposure to VPA in utero leads to brain abnormalities similar than those reported in the autistic brain. Particularly, VPA reduces the number of Purkinje neurons in the rat cerebellum parallel to cerebellar abnormalities found in autism. Thus, we injected pregnant females on embryonic day 12 either with VPA (600mg/kg, i.p.) or 0.9% saline solution and obtained the cerebellum from their offspring at different postnatal time points. Testosterone has been linked to autism and plays an important role during brain development. Therefore, we identified and analyzed the androgen receptor (AR) by immunohistochemistry and densitometry, respectively. We found VPA decreases AR density in the superficial Purkinje layer only in cerebellar lobule 8 at PN7, but increased it at PN14 compared to control in males. In females, VPA decreased AR density in the superficial Purkinje layer in cerebellar lobule 6 at PN14, but increased it in lobule 9 at the same time point. No differences were found in the deep Purkinje layer of any cerebellar lobule in terms of AR density neither in males nor females. We additionally found a particular AR density decreasing in both superficial and deep regions across development in the majority of cerebellar lobules in males, but in all cerebellar lobules in females. Thus, our results indicate that VPA disrupts the AR ontogeny in the developing cerebellum in an age and region specific manner in male and female rats. Future epigenetic studies including the evaluation of histone deacetylases (HDAC's) might shed light these results as HDAC's are expressed by Purkinje neurons, interact with the AR and are VPA targets. This work contributes to the understanding of the cerebellar development and it might help to understand the role of the cerebellum in neurodevelopmental disorders such as autism.
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PMID:Prenatal exposure to sodium valproate alters androgen receptor expression in the developing cerebellum in a region and age specific manner in male and female rats. 2742 76