Preprint Article Version 1 This version is not peer-reviewed

Pathogenicity of Endocrine Dysregulation in Autism

Version 1 : Received: 23 May 2018 / Approved: 25 May 2018 / Online: 25 May 2018 (10:37:23 CEST)

How to cite: Swierczynski, A.J.. Pathogenicity of Endocrine Dysregulation in Autism. Preprints 2018, 2018050359 (doi: 10.20944/preprints201805.0359.v1). Swierczynski, A.J.. Pathogenicity of Endocrine Dysregulation in Autism. Preprints 2018, 2018050359 (doi: 10.20944/preprints201805.0359.v1).

Abstract

The voluminous daily output of autism research has become increasingly disconnected, existing largely within highly specific subspecialty areas, and lacking cross-disciplinary linkages of context, theory, and findings to inform a unified body of knowledge. Robust syntheses of published research across the fields of psychiatry, cellular and molecular biology, neurology, endocrinology, immunology, behavioral and social sciences, and pedagogy may help clarify and extend current knowledge by guiding more efficient future research efforts investigating underlying causes, developmental divergences, novel treatments, and specific, sensitive biological markers in autism. This synthesis of interdisciplinary research indicates the hypothalamic-pituitary-adrenal (HPA) stress axis may be at the center of an interaction among sex steroids, immune function, signaling protein transcriptions, neurogenesis, and dysregulation of brain structures sending or receiving projections from the HPA stress axis. These interaction manifest observably as a range of sexually dimorphic behaviors and functional limitations often falling within the current diagnostic features of Autism Spectrum Disorder (ASD). The pathogenicity of endocrine dysregulation may serve as a valuable model for developing a cohesive theory of ASD by explaining how the HPA and connected brain areas respond to extreme conditions of dysregulated endocrine signaling to cause symptoms associated with autism.

Subject Areas

autism spectrum disorder; endocrine; estrogen; immune activation; melanin concentrating hormone

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