The pathogenesis of autism.

Clinical medicine. Pathology Pub Date : 2008-01-01 Epub Date: 2008-09-18 DOI:10.4137/cpath.s1143
Timothy John Watts
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Abstract

Autism is well known as a complex developmental disorder with a seemingly confusing and uncertain pathogenesis. The definitive mechanisms that promote autism are poorly understood and mostly unknown, yet available theories do appear to focus on the disruption of normal cerebral development and its subsequent implications on the functional brain unit. This mini-review aims solely to discuss and evaluate the most prominent current theories regarding the pathogenesis of autism. The main conclusion is that although there is not a clear pathway of mechanisms directed towards a simple pathogenesis and an established link to autism on the symptomatic level; there are however several important theories (neural connectivity, neural migration, excitatory-inhibitory neural activity, dendritic morphology, neuroimmune; calcium signalling and mirror neurone) which appear to offer an explanation to how autism develops. It seems probable that autism's neurodevelopmental defect is 'multi-domain' in origin (rather than a single anomaly) and is hence distributed across numerous levels of study (genetic, immunopathogenic, etc.). A more definitive understanding of the pathogenesis could facilitate the development of better treatments for this complex psychiatric disorder.

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自闭症的发病机理。
众所周知,自闭症是一种复杂的发育障碍,其发病机制看似混乱且不确定。人们对自闭症的确切发病机制知之甚少,大多不得而知,但现有的理论似乎都集中在大脑正常发育的破坏及其对大脑功能单元的影响上。本微型综述的唯一目的是讨论和评估当前有关自闭症发病机制的最主要理论。主要结论是,虽然在简单的发病机制方面没有明确的途径,在症状方面也没有与自闭症建立联系,但有几个重要的理论(神经连接、神经迁移、兴奋-抑制神经活动、树突形态、神经免疫、钙信号和镜像神经元)似乎可以解释自闭症是如何发展的。自闭症的神经发育缺陷很可能起源于 "多领域"(而非单一异常),因此分布于多个研究层面(遗传、免疫致病等)。对自闭症发病机理更明确的认识有助于开发出治疗这种复杂精神疾病的更好方法。
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