Marotta Rosa, Risoleo Maria C, Messina Giovanni, Parisi Lucia, Carotenuto Marco, Vetri Luigi, Roccella Michele
Department of Medical and Surgical Sciences, University "Magna Graecia", Catanzaro 88100, Italy.
Clinic of Child and Adolescent Neuropsychiatry, Department of Mental Health, Physical and Preventive Medicine, University of Campania "Luigi Vanvitelli", Napoli 80138, Italy.
Brain Sci. 2020 Mar 13;10(3):163. doi: 10.3390/brainsci10030163.
Autism spectrum disorder (ASD) refers to complex neurobehavioral and neurodevelopmental conditions characterized by impaired social interaction and communication, restricted and repetitive patterns of behavior or interests, and altered sensory processing. Environmental, immunological, genetic, and epigenetic factors are implicated in the pathophysiology of autism and provoke the occurrence of neuroanatomical and neurochemical events relatively early in the development of the central nervous system. Many neurochemical pathways are involved in determining ASD; however, how these complex networks interact and cause the onset of the core symptoms of autism remains unclear. Further studies on neurochemical alterations in autism are necessary to clarify the early neurodevelopmental variations behind the enormous heterogeneity of autism spectrum disorder, and therefore lead to new approaches for the treatment and prevention of autism. In this review, we aim to delineate the state-of-the-art main research findings about the neurochemical alterations in autism etiology, and focuses on gamma aminobutyric acid (GABA) and glutamate, serotonin, dopamine, N-acetyl aspartate, oxytocin and arginine-vasopressin, melatonin, vitamin D, orexin, endogenous opioids, and acetylcholine. We also aim to suggest a possible related therapeutic approach that could improve the quality of ASD interventions. Over one hundred references were collected through electronic database searching in Medline and EMBASE (Ovid), Scopus (Elsevier), ERIC (Proquest), PubMed, and the Web of Science (ISI).
自闭症谱系障碍(ASD)是指复杂的神经行为和神经发育状况,其特征为社交互动和沟通受损、行为或兴趣模式受限且重复,以及感觉加工改变。环境、免疫、遗传和表观遗传因素与自闭症的病理生理学有关,并在中枢神经系统发育的相对早期引发神经解剖学和神经化学事件。许多神经化学通路参与了自闭症的决定过程;然而,这些复杂网络如何相互作用并导致自闭症核心症状的发作仍不清楚。有必要对自闭症中的神经化学改变进行进一步研究,以阐明自闭症谱系障碍巨大异质性背后的早期神经发育变化,从而找到治疗和预防自闭症的新方法。在本综述中,我们旨在阐述关于自闭症病因中神经化学改变的最新主要研究发现,并重点关注γ-氨基丁酸(GABA)和谷氨酸、血清素、多巴胺、N-乙酰天门冬氨酸、催产素和精氨酸加压素、褪黑素、维生素D、食欲素、内源性阿片类物质和乙酰胆碱。我们还旨在提出一种可能相关的治疗方法,以提高自闭症干预措施的质量。通过在Medline和EMBASE(Ovid)、Scopus(Elsevier)、ERIC(Proquest)、PubMed和科学网(ISI)中进行电子数据库搜索,收集了一百多篇参考文献。