Laboratory of Cognitive and Computational Neuroscience, Center for Biomedical Technology, Technical University of Madrid, Madrid, Comunidad de Madrid 28223, Spain.
Department of Experimental Psychology, Universidad Complutense de Madrid, Madrid, Comunidad de Madrid 28223, Spain.
Cereb Cortex. 2021 Jan 5;31(2):1201-1210. doi: 10.1093/cercor/bhaa286.
Alzheimer's disease (AD) studies on animal models, and humans showed a tendency of the brain tissue to become hyperexcitable and hypersynchronized, causing neurodegeneration. However, we know little about either the onset of this phenomenon or its early effects on functional brain networks. We studied functional connectivity (FC) on 127 participants (92 middle-age relatives of AD patients and 35 age-matched nonrelatives) using magnetoencephalography. FC was estimated in the alpha band in areas known both for early amyloid accumulation and disrupted FC in MCI converters to AD. We found a frontoparietal network (anterior cingulate cortex, dorsal frontal, and precuneus) where relatives of AD patients showed hypersynchronization in high alpha (not modulated by APOE-ε4 genotype) in comparison to age-matched nonrelatives. These results represent the first evidence of neurophysiological events causing early network disruption in humans, opening a new perspective for intervention on the excitation/inhibition unbalance.
阿尔茨海默病（AD）在动物模型和人类中的研究表明，脑组织趋向于过度兴奋和过度同步，导致神经退行性变。然而，我们对这种现象的开始或其对功能大脑网络的早期影响知之甚少。我们使用脑磁图研究了 127 名参与者（92 名 AD 患者的中年亲属和 35 名年龄匹配的非亲属）的功能连接（FC）。在已知早期淀粉样蛋白积累和 MCI 转化为 AD 时 FC 中断的区域，在 alpha 波段估计了 FC。我们发现了一个额顶网络（前扣带回皮层、背侧额叶和楔前叶），在 AD 患者的亲属中，与年龄匹配的非亲属相比，高 alpha 频段表现出过度同步（不受 APOE-ε4 基因型调节）。这些结果代表了在人类中引起早期网络破坏的神经生理事件的第一个证据，为兴奋/抑制失衡的干预开辟了新的视角。
