Verma Ajay K, Nandakumar Bharadwaj, Acedillo Kit, Yu Ying, Marshall Ethan, Schneck David, Fiecas Mark, Wang Jing, MacKinnon Colum D, Howell Michael J, Vitek Jerrold L, Johnson Luke A
Department of Neurology, University of Minnesota, Minneapolis, MN, United States.
Masonic Institute for the Developing Brain, University of Minnesota, Minneapolis, MN, United States.
Front Neurosci. 2024 Feb 21;18:1338624. doi: 10.3389/fnins.2024.1338624. eCollection 2024.
Increasing evidence suggests slow-wave sleep (SWS) dysfunction in Parkinson's disease (PD) is associated with faster disease progression, cognitive impairment, and excessive daytime sleepiness. Beta oscillations (8-35 Hz) in the basal ganglia thalamocortical (BGTC) network are thought to play a role in the development of cardinal motor signs of PD. The role cortical beta oscillations play in SWS dysfunction in the early stage of parkinsonism is not understood, however. To address this question, we used a within-subject design in a nonhuman primate (NHP) model of PD to record local field potentials from the primary motor cortex (MC) during sleep across normal and mild parkinsonian states. The MC is a critical node in the BGTC network, exhibits pathological oscillations with depletion in dopamine tone, and displays high amplitude slow oscillations during SWS. The MC is therefore an appropriate recording site to understand the neurophysiology of SWS dysfunction in parkinsonism. We observed a reduction in SWS quantity ( = 0.027) in the parkinsonian state compared to normal. The cortical delta (0.5-3 Hz) power was reduced ( = 0.038) whereas beta (8-35 Hz) power was elevated ( = 0.001) during SWS in the parkinsonian state compared to normal. Furthermore, SWS quantity positively correlated with delta power ( = 0.43, = 0.037) and negatively correlated with beta power ( = -0.65, < 0.001). Our findings support excessive beta oscillations as a mechanism for SWS dysfunction in mild parkinsonism and could inform the development of neuromodulation therapies for enhancing SWS in people with PD.
越来越多的证据表明，帕金森病（PD）中的慢波睡眠（SWS）功能障碍与疾病进展加快、认知障碍和日间过度嗜睡有关。基底神经节丘脑皮质（BGTC）网络中的β振荡（8 - 35Hz）被认为在PD主要运动症状的发展中起作用。然而，皮质β振荡在帕金森病早期SWS功能障碍中所起的作用尚不清楚。为了解决这个问题，我们在PD的非人灵长类动物（NHP）模型中采用了受试者内设计，以记录正常和轻度帕金森状态下睡眠期间初级运动皮层（MC）的局部场电位。MC是BGTC网络中的一个关键节点，随着多巴胺能降低会出现病理性振荡，并且在SWS期间表现出高振幅慢振荡。因此，MC是了解帕金森病中SWS功能障碍神经生理学的合适记录部位。我们观察到，与正常状态相比，帕金森状态下SWS的量减少了（ = 0.027）。与正常状态相比，帕金森状态下SWS期间皮质δ波（0.5 - 3Hz）功率降低（ = 0.038），而β波（8 - 35Hz）功率升高（ = 0.001）。此外，SWS的量与δ波功率呈正相关（ = 0.43， = 0.037），与β波功率呈负相关（ = -0.65， < 0.001）。我们的研究结果支持过度的β振荡是轻度帕金森病中SWS功能障碍的一种机制，并可为开发用于增强PD患者SWS的神经调节疗法提供依据。
