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 interactions 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.
Highlights
The neuro-developmental disorder of Autism has generated perplexed reactions from the scientific community for nearly 80 years since Leo Kanner [116] first distinguished a set of “feebleminded” (p. 242) children with unique observable characteristics
This paper provides an interdisciplinary integration of knowledge addressing the epidemiology of autism spectrum disorders (ASD)
This biopsychosocial perspective has identified excessive signaling of estrogens and melanin-concentrating hormone system (MCH), producing HPA axis hyperactivation and inflammatory cytokine expression. These cytokines are capable of modulating a positive feedback loop via COX-2 up-regulating prostaglandin E2 (PGE2), resulting in higher transcription of aromatase, followed by increased estrogen expression
Summary
The neuro-developmental disorder of Autism has generated perplexed reactions from the scientific community for nearly 80 years since Leo Kanner [116] first distinguished a set of “feebleminded” (p. 242) children with unique observable characteristics. Kanner borrowed the word ‘autistic’ from a description of the state of mind observed in patients with schizophrenia who were seemingly lost in their internal world with little consideration for the shared, external world117 in order to separate this population clinically from other feebleminded children. While autism has been recognized as a unique developmental disorder since Kanner’s seminal descriptions, frequent redefinitions and revised conceptualizations of the condition have contributed to subsequent and persisting uncertainties about the nature of ASD and the identification of universally effective treatments. Each discipline uses its own paradigms and corresponding language to describe interactions between an organism and its environment. This often leads to very important details being misunderstood, or lost
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