Department of Human Physiology, University of Oregon, Eugene, Oregon, United States.
Department of Sport, Exercise and Rehabilitation, Northumbria University, Newcastle Upon Tyne, United Kingdom.
J Neurophysiol. 2023 May 1;129(5):1086-1093. doi: 10.1152/jn.00480.2022. Epub 2023 Apr 5.
Aging is a key risk factor for the development of Parkinson's disease (PD). PD is characterized by excessive synchrony of beta oscillations (13-30 Hz) in the basal ganglia thalamo-cortical network. However, cortical beta power is not reliably elevated in individuals with PD. Here, we sought to disentangle how resting cortical beta power compares in younger controls, older controls, and individuals with PD using scalp electroencephalogram (EEG) and a novel approach for quantifying beta power. Specifically, we used a Gaussian model to determine if sensorimotor beta power distinguishes these groups. In addition, we looked at the distribution of beta power across the entire cortex. Our findings showed that Gaussian-modeled beta power does not differentiate individuals with PD (on medication) from healthy younger or older controls in sensorimotor cortex. However, beta power (and not theta or alpha) was higher in healthy older versus younger controls. This effect was most pronounced in regions near sensorimotor cortex including the frontal and parietal areas [ < 0.05, false discovery rate (FDR) corrected]. In addition, the bandwidth of the periodic beta was also higher in healthy older than young individuals in parietal regions. Finally, the aperiodic component, specifically the exponent of the signal, was higher (steeper) in younger controls than in individuals with PD in the right parietal-occipital region ( < 0.05, FDR corrected), possibly reflecting differences in neuronal spiking. Our findings suggest that cortical Gaussian beta power is possibly modulated by age and could be further explored in longitudinal studies to determine whether sensorimotor beta increases with increasing age. Altered sensorimotor beta activity has been shown to be a feature in aging and PD. Using a novel approach, we clarify that resting sensorimotor beta power does not distinguish subjects with PD from healthy younger and older controls. However, beta power was higher in older compared with younger controls in central sensorimotor, frontal, and parietal regions. These results provide a clearer picture of sensorimotor beta power, demonstrating that it is elevated in aging but not PD.
衰老(aging)是帕金森病(Parkinson's disease,PD)发生的关键风险因素。PD 的特征是基底神经节丘脑皮质网络中的β振荡(13-30Hz)过度同步。然而,在 PD 患者中,皮质β波的功率并没有可靠地升高。在这里,我们试图使用头皮脑电图(electroencephalogram,EEG)和一种新的方法来量化β波功率,来厘清在年轻对照组、老年对照组和 PD 患者中,静息皮质β波功率的差异。具体来说,我们使用高斯模型来确定感觉运动β波功率是否可以区分这些组。此外,我们还观察了整个皮质的β波功率分布。我们的研究结果表明,在感觉运动皮质中,高斯模型化的β波功率并不能区分服用药物的 PD 患者与健康的年轻或老年对照组。然而,与健康的年轻对照组相比,健康的老年对照组的β波功率(而不是θ波或α波)更高。这种效应在靠近感觉运动皮质的区域最为明显,包括额叶和顶叶区域[ < 0.05,经假发现率(false discovery rate,FDR)校正]。此外,与年轻个体相比,健康老年人的顶叶区域的周期性β带宽也更高。最后,与 PD 患者相比,右侧顶枕叶区域的无周期性成分(具体为信号指数)在年轻对照组中更高(更陡峭)[ < 0.05,经 FDR 校正],这可能反映了神经元放电的差异。我们的研究结果表明,皮质高斯β波功率可能受到年龄的调节,并可以在纵向研究中进一步探索,以确定感觉运动β波是否随着年龄的增长而增加。感觉运动β活动的改变已被证明是衰老和 PD 的一个特征。使用一种新的方法,我们阐明了静息感觉运动β波功率不能将 PD 患者与健康的年轻和老年对照组区分开来。然而,与年轻对照组相比,老年对照组在中央感觉运动、额叶和顶叶区域的β波功率更高。这些结果提供了更清晰的感觉运动β波功率图,表明其在衰老中升高,但在 PD 中不升高。