enhanced gamma activity and cross-frequency interaction of resting-state electroencephalographic oscillations in patients with alzheimer’s disease

enhanced gamma activity and cross-frequency interaction of resting-state electroencephalographic oscillations in patients with alzheimer’s disease

;Jing Wang;Jing Wang;Jing Wang;Yuxing Fang;Xiao Wang;Xiao Wang;Xiao Wang;Huichao Yang;Huichao Yang;Xin Yu;Xin Yu;Xin Yu;Huali Wang;Huali Wang;Huali Wang
Frontiers in chemistry 2017 Vol. 9 pp. -
166
wang2017frontiersenhanced

Abstract

Cognitive impairment, functional decline and behavioral symptoms that characterize Alzheimer’s disease (AD) are associated with perturbations of the neuronal network. The typical electroencephalographic (EEG) features in AD patients are increased delta or theta rhythm and decreased alpha or beta rhythm activities. However, considering the role of cross-frequency couplings in cognition, the alternation of cross-frequency couplings in AD patients is still obscure. This study aims to explore the interaction dynamics between different EEG oscillations in AD patients. We recorded the resting eye-closed EEG signals in 8 AD patients and 12 healthy volunteers. By analyzing the wavelet power spectrum and bicoherence of EEG, we found enhanced gamma rhythm power in AD patients in addition to the increased delta and decreased alpha power. Furthermore, an enhancement of the cross-frequency coupling strength between the beta/gamma and low-frequency bands was observed in AD patients compared to healthy controls (HCs). We propose that the pathological increase of ongoing gamma-band power might result from the disruption of the GABAergic interneuron network in AD patients. Furthermore, the cross-frequency overcouplings, which reflect the enhanced synchronization, might indicate the attenuated complexity of the neuronal network, and AD patients have to use more neural resources to maintain the resting brain state. Overall, our findings provide new evidence of the disturbance of the brain oscillation network in AD and further deepen our understanding of the central mechanisms of AD.

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221201
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10.3389/fnagi.2017.00243
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