In Parkinson's disease (PD) patients, beta (β) and gamma (γ) oscillations are altered in the basal ganglia, and this abnormality contributes to the pathophysiology of bradykinesia. However, it is unclear whether β and γ rhythms at the primary motor cortex (M1) level influence bradykinesia. Transcranial alternating current stimulation (tACS) can modulate cortical rhythms by entraining endogenous oscillations. We tested whether β- and γ-tACS on M1 modulate bradykinesia in PD patients by analyzing the kinematic features of repetitive finger tapping, including movement amplitude, velocity, and sequence effect, recorded during β-, γ-, and sham tACS. We also verified whether possible tACS-induced bradykinesia changes depended on modifications in specific M1 circuits, as assessed by short-interval intracortical inhibition (SICI) and short-latency afferent inhibition (SAI). Patients were studied OFF and ON dopaminergic therapy. Results were compared to those obtained in a group of healthy subjects (HS). In patients, movement velocity significantly worsened during β-tACS and movement amplitude improved during γ-tACS, while the sequence effect did not change. In addition, SAI decreased (reduced inhibition) during β-tACS and SICI decreased during both γ- and β-tACS in PD. The effects of tACS were comparable between OFF and ON sessions. In patients OFF therapy, the degree of SICI modulation during β- and γ-tACS correlated with movement velocity and amplitude changes. Moreover, there was a positive correlation between the effect of γ-tACS on movement amplitude and motor symptoms severity. Our results show that cortical β and γ oscillations are relevant in the pathophysiology of bradykinesia in PD and that changes in inhibitory GABA-A-ergic interneuronal activity may reflect compensatory M1 mechanisms to counteract bradykinesia. In conclusion, abnormal oscillations at the M1 level of the basal ganglia-thalamo-cortical network play a relevant role in the pathophysiology of bradykinesia in PD.