有关小脑在自闭症病因中的作用的科学知识的各个方面都取得了重大进展。在当前的共识文件中,我们将观察关于自闭症病理中这个重要部位的不同意见。讨论了与小脑参与自闭症有关的文献中的最新发现,包括:小脑病理学,自闭症的小脑成像和症状表达,小脑遗传学,小脑免疫功能,氧化应激和线粒体功能障碍,GABA能和谷氨酸能系统,胆碱能,多巴胺能,血清素能,和催产素相关的自闭症改变,运动控制和认知缺陷,小脑运动和认知的协调,基因-环境相互作用,自闭症的治疗方法,和相关的自闭症动物模型。共识点包括存在异常的小脑解剖结构,异常的神经递质系统,氧化应激,小脑运动和认知缺陷,自闭症患者的神经炎症。不确定的领域或需要进一步调查的领域包括缺乏针对自闭症核心症状的治疗方案,口腔发育不全,和其他作为自闭症一贯特征的畸形,小脑对认知的潜在贡献机制,神经炎症的潜在机制未知。
There has been significant advancement in various aspects of scientific knowledge concerning the role of cerebellum in the etiopathogenesis of autism. In the current
consensus paper, we will observe the diversity of opinions regarding the involvement of this important site in the pathology of autism. Recent emergent findings in literature related to cerebellar involvement in autism are discussed, including: cerebellar pathology, cerebellar imaging and symptom expression in autism, cerebellar genetics, cerebellar immune function, oxidative stress and mitochondrial dysfunction, GABAergic and glutamatergic systems, cholinergic, dopaminergic, serotonergic, and oxytocin-related changes in autism, motor control and cognitive deficits, cerebellar coordination of movements and cognition, gene-environment interactions, therapeutics in autism, and relevant animal models of autism. Points of
consensus include presence of abnormal cerebellar anatomy, abnormal neurotransmitter systems, oxidative stress, cerebellar motor and cognitive deficits, and neuroinflammation in subjects with autism. Undefined areas or areas requiring further investigation include lack of treatment options for core symptoms of autism, vermal hypoplasia, and other vermal abnormalities as a consistent feature of autism, mechanisms underlying cerebellar contributions to cognition, and unknown mechanisms underlying neuroinflammation.