Bing-Yu Li, Ruo-Yu Li, Rong-Hua Hong, Yun-Ping Song, Ling-Jing Jin
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.