物理学进展

物理学进展 ›› 2025, Vol. 45 ›› Issue (6): 261-280.doi: 10.13725/j.cnki.pip.2025.06.001

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自闭症谱系障碍与注意力缺陷多动障碍共病的潜在机制

余 晨 1, 2，张小鹏 2, 3∗，王 炜 1, 3†   

  1. 1. 南京大学物理学院，固体微结构国家实验室，南京 210093 2. 南京大学匡亚明学院，南京 210023 3. 南京大学脑科学研究院，南京 210023
  • 出版日期:2025-12-20 发布日期:2026-01-05
  • 基金资助:
    国家自然科学基金项目 (12090052)、南京大学心智发展与脑功能研究基金

Potential mechanisms of comorbidity between autism spectrum disorder and attention deficit hyperactivity disorder

YU Chen 1, 2, ZHANG Xiaopeng 2, 3∗ , WANG Wei 1, 3†    

  1. 1. National Laboratory of Solid State Microstructuresm, School of Physics, Nanjing University, Nanjing 210093, China 2. Kuang Yaming Honors School, Nanjing University, Nanjing 210023, China 3. Institute for Brain Sciences, Nanjing University, Nanjing 210023, China
  • Online:2025-12-20 Published:2026-01-05

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摘要：

自闭症谱系障碍 (自闭症) 与注意力缺陷多动障碍 (多动症) 是儿童常患的神经发育障碍类 疾病，二者表现出截然不同的症状，但却具有很高的共病概率。本文将从神经生物物理学角度梳 理不同层次的研究进展，系统总结自闭症与多动症共病的生物物理机制。儿童共患两种疾病的机 理可概括为以下几个方面：(1) 两种疾病均存在突触修剪异常，导致共病患者的脑结构异常加剧； (2) 脑网络功能障碍是二者共病的重要神经生物学证据；(3) 二者均涉及多巴胺、Wnt、γ-氨基丁 酸、雷帕霉素靶蛋白和炎症相关信号通路的异常，这些通路与突触数量的稳定性紧密相关；(4) 突 触修剪异常导致的突触兴奋性/抑制性失衡是共患两种疾病的基本原因。此外，借助计算神经网络 建模和分子网络动力学建模，可促进对自闭症与多动症共病机制的深入理解。本文从不同层次分 析了两种典型神经发育障碍出现共病的潜在机制，有望为共病患者的早期干预和精准治疗提供理 论依据。

关键词: 自闭症谱系障碍, 注意力缺陷多动障碍, 生物物理机制, 信号通路, 突触修剪, 理论建 模

Abstract:

Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) exhibit a high rate of comorbidity. This paper systematically reviews existing studies at different levels to summarize the common pathological mechanisms underlying the comorbidity of ASD and ADHD. Specifically: (1) Both diseases exhibit abnormal synaptic pruning, leading to a further aggravation of abnormal brain structure in patients with the comorbidity; (2) Dysfunction of the default mode network and executive control network constitutes important neurobiological evidence for the comorbidity of the two disorders; (3) The abnormal signaling pathways implicated in ASD and ADHD mainly involve the dopamine, Wnt, GABA, mTOR, and inflammation-related pathways, all of which are closely associated with the stability of synapse numbers; (4) Abnormal synaptic pruning leads to excitatory/inhibitory (E/I) imbalance, which may provide the physiological basis for abnormal functional connectivity of brain networks and altered cortical thickness and volume in higher cognitive regions such as the prefrontal cortex. Moreover, by computational neural network modeling and molecular network modeling, it is expected to advance the understanding of the co-morbidity mechanism of autism and attention deficit hyperactivity disorder. In this review, we elucidate the pathological mechanism of comorbidity in two typical diseases related to neurodevelopmental disorders from different perspectives, and may provide a theoretical basis for early intervention and precise treatment in comorbid patients.

Key words: autism spectrum disorder, attention deficit hyperactivity disorder, biophysical mechanism, signaling pathway, synaptic pruning, theoretical modeling

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