This chapter reviews that the core pathology of PD is degeneration of the dopamine neurons in the midbrain and the resulting depletion of striatal dopamine. The striatum is the major input stage of the basal ganglia, receiving input from the cerebral cortex and thalamus, and projecting directly and indirectly to the output stages of the basal ganglia – the internal segment of the globus pallidus (GPi) and the substantia nigra pars reticulata (SNr). The dopamine precursor l-DOPA remains the gold standard for the treatment of PD. However, long-term use of l-DOPA is associated with the development of motor complications. It discusses that the multi-stage therapy of Parkinson's disease (PD), from dopamine replacement methods to modulation of the activity of the basal ganglia structures using deep Brain Stimulation DBS, reinstates interest in identifying the critical features of abnormal basal ganglia activity that follow striatal dopamine depletion and lead to the symptoms. The chapter summarizes the main physiological findings in the 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) primate model of PD, and compares them to the recent physiological findings in human patients. There is an accumulation of data linking excessive synchrony at low frequencies in basal ganglia-thalamo-cortical loops to impaired motor processing in PD. Whether synchronization is an epiphenomenon or truly pathogenic in PD, it provides a clear biological marker for the disease process. Recent studies indicate the differential roles or correlates of the distinctive bands of oscillatory activity in the pathogenesis of PD. It suggests that amelioration of specific domains of basal ganglia-cortical synchronized oscillatory activity could form the basis for future closed-loop stimulation regimes for human PD patients.