Bing‑Yu Li1  · Ruo‑Yu Li1,2 · Rong‑Hua Hong1,2  · Yun‑Ping Song1  · Ling‑Jing Jin1,2,3,4

1 Department of Neurology and Neurological Rehabilitation, Shanghai Disabled Persons’ Federation Key Laboratory of Intelligent Rehabilitation Assistive Devices and Technologies, Yangzhi Rehabilitation Hospital (Shanghai Sunshine Rehabilitation Center), School of Medicine, Tongji University, Shanghai 201619, China 

2 Neurotoxin Research Center, Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Department of Neurology, Tongji Hospital, School of Medicine, Tongji University, Shanghai 200065, China 

3 Collaborative Innovation Center for Brain Science, Tongji University, Shanghai 200092, China 

4 Shanghai Key Laboratory of Wearable Robotics and Human-Machine Interaction, Shanghai 201804, China

Abstract

Parkinson’s disease (PD) is the second-most prevalent neurodegenerative disorder, with no definitive cure currently available. Within the basal ganglia–thalamocortical circuitry, PD is characterized by an imbalance between antikinetic beta oscillations (13–35 Hz) and prokinetic gamma oscillations (60–90 Hz). While the pathological features and mechanisms underlying abnormal beta activity have been extensively studied, alterations in gamma oscillations remain much less well understood. Emerging evidence indicates that different forms of gamma activity are disrupted in PD and associated with symptoms such as dyskinesia, gait impairment, and rapid eye movement (REM) sleep behavior disorder. This review summarizes current clinical and preclinical evidence of aberrant gamma oscillations in PD, discusses underlying mechanisms including parvalbumin interneuron dysfunction, basal ganglia circuit imbalance, and impaired neurovascular coupling, and summarizes how current therapeutic approaches for PD modulate gamma activity and potentially influence clinical outcomes.

Keywords

Gamma oscillations; Neural oscillation; Parkinson’s disease

[SpringerLink]