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- W1963509955 abstract "The phenotypic expression of autism spectrum disorders varies widely in severity and characteristics and it is, therefore, likely that a number of etiological factors are involved. However, one finding which has been found consistently is that there is a greater incidence of autism in boys than girls. Recently, attention has been given to the extreme male hypothesis-that is that autism behaviors are an extreme form of typical male behaviors, including lack of empathy and language deficits but an increase in so-called systemizing behaviors, such as attention to detail and collecting. This points to the possibility that an alteration during sexual differentiation of the brain may occur in autism. During sexual differentiation of the brain, two brain regions are highly sexually dimorphic-the amygdala and the hypothalamus. Both of these regions are also implicated in the neuroendocrine hypothesis of autism, wherein a balance between oxytocin and cortisol may contribute to the disorder. We are thus proposing that the extreme male hypothesis and the neuroendocrine hypothesis are in fact compatible in that sexual differentiation of the brain towards an extreme male phenotype would result in the neuroendocrine changes proposed in autism. We have preliminary data, treating developing rat pups with the differentiating hormone 17-β estradiol during a critical time and showing changes in social behaviors and oxytocin, to support this hypothesis. Further studies should be undertaken to confirm the role of extremes of normal sexual differentiation in producing the neuroendocrine changes associated with autism." @default.
- W1963509955 created "2016-06-24" @default.
- W1963509955 creator A5069253641 @default.
- W1963509955 creator A5089249810 @default.
- W1963509955 date "2011-09-08" @default.
- W1963509955 modified "2023-09-23" @default.
- W1963509955 title "Sexual Differentiation and the Neuroendocrine Hypothesis of Autism" @default.
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- W1963509955 doi "https://doi.org/10.1002/ar.21251" @default.
- W1963509955 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21901838" @default.
- W1963509955 hasPublicationYear "2011" @default.
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