Intrinsic connectivity identifies the sensory-motor network as a main cross-network between remitted late-life depression- and amnestic mild cognitive impairment-targeted networks
Intrinsic connectivity identifies the sensory-motor network as a main cross-network between remitted late-life depression- and amnestic mild cognitive impairment-targeted networks
复制标题
内在连接将感觉运动网络识别为缓解晚年抑郁症和遗忘性轻度认知障碍目标网络之间的主要交叉网络
DOI：
10.1007/s11682-019-00098-4
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发表时间：
2020-08-01
影响因子：
3.2
通讯作者：
Zhang, Zhijun
中科院分区：
文献类型：
--
作者：
Chen, Jiu;Shu, Hao;Zhang, Zhijun
老年抑郁症缓解（rLLD）和遗忘型轻度认知障碍（aMCI）都与阿尔茨海默病（AD）的高风险相关。神经退化被认为是在预先存在的网络中传播的。为了研究在健康的大脑中，在易受rLLD和aMCI影响的内在网络之间是否存在预先存在的交叉网络。我们在55例rLLD、87例aMCI和114例健康对照者中，根据脑神经元活动差异最大的脑区进行了功能连接分析。在健康大脑中，对rLLD和aMCI有不同脆弱性的内在网络会聚到感觉运动网络（SMN）上。这些区域在SMN的aMCI和rLLD脆弱的网络在认知功能中发挥不同的作用。这项研究确定了SMN作为rLLD和aMCI脆弱网络之间的交叉网络。这些疾病对AD的共同易感性可能是由于交叉网络的崩溃。结果进一步表明，在AD风险个体的疾病早期，针对改善感觉运动缺陷的干预措施可能会随着AD病理学进展而增强患者的功能。
Remitted late-life depression (rLLD) and amnestic mild cognitive impairment (aMCI) are both associated with a high risk of developing Alzheimer's disease (AD). Neurodegeneration is considered to spread within pre-existing networks. To investigate whether, in the healthy brain, there was a pre-existing cross-network between the intrinsic networks that are vulnerable to rLLD and aMCI. We performed functional connectivity analyses based on brain areas with the greatest brain neuronal activity differences in 55 rLLD, 87 aMCI, and 114 healthy controls. Intrinsic networks that were differentially vulnerable to rLLD and aMCI converged onto the sensory-motor network (SMN) in the healthy brain. These regions in the SMN within the aMCI- and rLLD-vulnerable networks played different roles in the cognitive functions. This study identifies the SMN as a cross-network between rLLD- and aMCI-vulnerable networks. The common susceptibility of these diseases to AD is likely due to the breakdown of the cross-network. The results further suggest that interventions targeting the amelioration of sensory-motor deficits in the early course of disease in individuals with AD risk may enhance patient function as AD pathology progresses.