A CRH Theory of Autism Spectrum Disorder

Ari Rappoport
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Abstract

This paper presents a complete theory of autism spectrum disorder (ASD), explaining its etiology, symptoms, and pathology. The core cause of ASD is excessive stress-induced postnatal release of corticotropin-releasing hormone (CRH). CRH competes with urocortins for binding to the CRH2 receptor, impairing their essential function in the utilization of glucose for growth. This results in impaired development of all brain areas depending on CRH2, including areas that are central in social development and eye gaze learning, and low-level sensory areas. Excessive CRH also induces excessive release of adrenal androgens (mainly DHEA), which impairs the long-term plasticity function of gonadal steroids. I show that these two effects can explain all of the known symptoms and properties of ASD. The theory is supported by strong diverse evidence, and points to very early detection biomarkers and preventive pharmaceutical treatments, one of which seems to be very promising.
自闭症谱系障碍的 CRH 理论
本文提出了自闭症谱系障碍(ASD)的完整理论,解释了其病因、症状和病理。自闭症谱系障碍(ASD)的核心病因是过度应激引起的产后促肾上腺皮质激素释放激素(CRH)释放。CRH 与尿皮质素竞争结合到 CRH2 受体上,损害了它们利用葡萄糖促进生长的基本功能。这导致所有依赖 CRH2 的脑区发育受损,其中包括社会发展和注视学习的核心区域以及低级感觉区域。过多的 CRH 还会诱导肾上腺雄激素(主要是 DHEA)的过度释放,从而损害雌激素的长期可塑性功能。我的研究表明,这两种效应可以解释所有已知的 ASD 症状和特性。该理论得到了各种有力证据的支持,并指出了非常早期的检测生物标志物和预防性药物疗法,其中一种疗法似乎很有前景。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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