PB is a chronic progressive neurodegenerative disease in which abnormal aggregates are deposited in the area of the pars compacta substantia nigra, leading to loss of dopaminergic neurons and striatal dopamine deficiency. It is the most common movement disorder and the second most common neurodegenerative disorder affecting as many as 2-3% of the population aged ≥65 years. The disease most often occurs between the ages of 65 and 70, and onset before the age of 40 is observed in less than 5% of cases. Unfortunately, the exact cause of PB is still unknown, but it is hypothesized that the disease could be multifactorial, involving genetic and environmental factors. The pathological feature of PB is the presence of abnormal intracytoplasmic inclusions, Lewy bodies that are constructed from the alpha-synuclein protein. The main motor symptoms of PB, also called cardinal, can be listed by the acronym TRAP, representing tremor at rest, rigidity, akinesia (or bradykinesia), and postural instability. In addition to motor symptoms, NMSs are present, such as sensory, neuropsychiatric, sleep and wakefulness disorders, and autonomic nervous system disorders. Levodopa has been the gold standard in the treatment of PB for 60 years. Although it has a good effect on most symptoms of PB, some symptoms are resistant to its application. Also, long-term use of levodopa leads to motor complications. Other conventional drugs are less effective and more difficult to tolerate, while older neurosurgical methods, thalamotomy and pallidotomy, have a significant risk of mortality and morbidity. Recent findings on the pathogenesis and genetics of PD have paved the way for developing new therapeutic methods. Numerous promising and innovative approaches have advanced to the stages of clinical trials and could be widely used in the clinic in a few years.