Consensus paper: pathological role of the cerebellum in autism.
Consensus paper: pathological role of the cerebellum in autism.
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DOI：
10.1007/s12311-012-0355-9
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发表时间：
2012-09
期刊：
影响因子：
3.5
通讯作者：
Welsh, John P.
中科院分区：
文献类型：
--
作者：
Fatemi, S. Hossein;Aldinger, Kimberly A.;Ashwood, Paul;Bauman, Margaret L.;Blaha, Charles D.;Blatt, Gene J.;Chauhan, Abha;Chauhan, Ved;Dager, Stephen R.;Dickson, Price E.;Estes, Annette M.;Goldowitz, Dan;Heck, Detlef H.;Kemper, Thomas L.;King, Bryan H.;Martin, Loren A.;Millen, Kathleen J.;Mittleman, Guy;Mosconi, Matthew W.;Persico, Antonio M.;Sweeney, John A.;Webb, Sara J.;Welsh, John P.
关键词：
关于小脑在自闭症病因发病机制中的作用，科学知识的各个方面都有了重大进展。在当前的共识性论文中，我们将看到关于这一重要部位在自闭症病理中所起作用的各种不同观点。文中讨论了近期文献中有关小脑参与自闭症的新发现，包括：小脑病理学、自闭症中的小脑成像及症状表现、小脑遗传学、小脑免疫功能、氧化应激与线粒体功能障碍、自闭症中γ -氨基丁酸能和谷氨酸能系统、胆碱能、多巴胺能、血清素能以及催产素相关变化、运动控制与认知缺陷、小脑对运动和认知的协调、基因 - 环境相互作用、自闭症的治疗方法以及相关的自闭症动物模型。共识要点包括自闭症患者存在小脑解剖结构异常、神经递质系统异常、氧化应激、小脑运动和认知缺陷以及神经炎症。未明确的领域或需进一步研究的领域包括缺乏针对自闭症核心症状的治疗方案、小脑蚓部发育不全及其他蚓部异常作为自闭症的一个一贯特征、小脑对认知贡献的潜在机制以及神经炎症的潜在未知机制。
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.
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