Neural connectivity abnormalities in autism: insights from the Tuberous Sclerosis model.
Neural connectivity abnormalities in autism: insights from the Tuberous Sclerosis model.
复制标题
DOI：
10.1186/1741-7015-11-55
复制
发表时间：
2013-02-27
期刊：
影响因子：
9.3
通讯作者：
Bolton P
中科院分区：
文献类型：
--
作者：
Tye C;Bolton P
自闭症谱系障碍（ASD）是一种由复杂的遗传和非遗传危险因素引起的行为综合征。有人提出，这些风险因素导致大脑回路的发育和“布线”发生变化，从而导致ASD的出现。虽然有几条研究路线支持这一理论，但病因学和临床异质性、方法学问题和不一致的发现导致了重大质疑。ASD的一个最好的建立，虽然罕见，原因是遗传性条件硬化症复杂（TSC），其中40%的人发展ASD。Peters和Taquet等人最近的一项研究使用图论分析了脑电图（EEG）数据，以模拟患有TSC伴和不伴ASD的个体以及患有“特发性”ASD的病例的神经“连接性”。TSC病例表现出全局连接不足和异常网络拓扑，而TSC + ASD个体表现出与特发性ASD个体相似的连接模式：长距离连接减少，短距离连接减少。TSC + ASD和ASD中连接异常的相似性表明了共同的最终通路，并为ASD中的“错误连接”神经回路提供了进一步的支持。连接变化的起源，以及它们在神经和认知/行为表现之间的中介作用，将需要进一步研究。请参阅相关的研究文章在这里http://www.biomedcentral.com/1741-7015/11/54
Autism Spectrum Disorder (ASD) is a behavioral syndrome caused by complex genetic and non-genetic risk factors. It has been proposed that these risk factors lead to alterations in the development and 'wiring' of brain circuits and hence, the emergence of ASD. Although several lines of research lend support to this theory, etiological and clinical heterogeneity, methodological issues and inconsistent findings have led to significant doubts. One of the best established, albeit rare, causes of ASD is the genetic condition Tuberous Sclerosis Complex (TSC), where 40% of individuals develop ASD. A recent study by Peters and Taquet et al. analyzed electroencephalography (EEG) data using graph theory to model neural 'connectivity' in individuals with TSC with and without ASD and cases with 'idiopathic' ASD. TSC cases exhibited global under-connectivity and abnormal network topology, whereas individuals with TSC + ASD demonstrated similar connectivity patterns to those seen in individuals with idiopathic ASD: decreased long- over short-range connectivity. The similarity in connectivity abnormalities in TSC + ASD and ASD suggest a common final pathway and provide further support for 'mis-wired' neural circuitry in ASD. The origins of the connectivity changes, and their role in mediating between the neural and the cognitive/behavioral manifestations, will require further study. Please see related research article here http://www.biomedcentral.com/1741-7015/11/54
登录
查看更多内容
DOI：
10.1523/jneurosci.2257-10.2010
发表时间：
2010-11-03
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Zikopoulos B;Barbas H
通讯作者：
Barbas H
影响因子：
64.8
作者：
Yizhar, Ofer;Fenno, Lief E.;Prigge, Matthias;Schneider, Franziska;Davidson, Thomas J.;O'Shea, Daniel J.;Sohal, Vikaas S.;Goshen, Inbal;Finkelstein, Joel;Paz, Jeanne T.;Stehfest, Katja;Fudim, Roman;Ramakrishnan, Charu;Huguenard, John R.;Hegemann, Peter;Deisseroth, Karl
通讯作者：
Deisseroth, Karl
影响因子：
5.3
作者：
Belmonte, MK;Allen, G;Webb, SJ
通讯作者：
Webb, SJ
影响因子：
4.8
作者：
Tsai, Peter;Sahin, Mustafa
通讯作者：
Sahin, Mustafa
影响因子：
14.5
作者：
Bolton, PF;Park, RJ;Pickles, A
通讯作者：
Pickles, A