Autism as a disorder of neural information processing: Directions for research and targets for therapy
Autism as a disorder of neural information processing: Directions for research and targets for therapy
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自闭症作为一种神经信息处理障碍：研究方向和治疗目标
DOI：
10.31234/osf.io/u4ehk
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发表时间：
2019
期刊：
影响因子：
--
通讯作者：
J. Rubenstein
中科院分区：
文献类型：
--
作者：
M. Belmonte;J. Rubenstein
自闭症谱系障碍的表型和严重程度的广泛变化表明涉及多种诱发因素，以复杂的方式与正常的发展过程和梯度相互作用。从因果因素到改变的大脑发育，以及从异常的大脑发育到改变的认知和行为的分歧，阻碍了对这些因素的识别，以及它们所进入的共同发展路径。关于自闭症的遗传学、神经化学、神经影像学和行为学研究结果，以及对正常发育和与自闭症症状相同的遗传综合征的研究，都提出了关于因果因素的性质及其对神经系统结构和动力学的可能影响的假设。神经特性的这种改变可能反过来扰乱活动依赖性发育，导致复杂的行为综合征，从根本原因出发需要许多步骤。基于遗传学、神经化学、神经生理学和行为学操作的动物模型提供了详细探索这些发育过程的可能性，人类研究也提供了超越诊断本身的内在表型。
The broad variation in phenotypes and severities within autism spectrum disorders suggests the involvement of multiple predisposing factors, interacting in complex ways with normal developmental courses and gradients. Identification of these factors, and the common developmental path into which they feed, is hampered by the large degrees of convergence from causal factors to altered brain development, and divergence from abnormal brain development into altered cognition and behaviour. Genetic, neurochemical, neuroimaging and behavioural findings on autism, as well as studies of normal development and of genetic syndromes that share symptoms with autism, offer hypotheses as to the nature of causal factors and their possible effects on the structure and dynamics of neural systems. Such alterations in neural properties may in turn perturb activity-dependent development, giving rise to a complex behavioural syndrome many steps removed from the root causes. Animal models based on genetic, neurochemical, neurophysiological, and behavioural manipulations offer the possibility of exploring these developmental processes in detail, as do human studies addressing endophenotypes beyond the diagnosis itself.