Parkinson disease (PD), among one of the most prevalent neurodegenerative illness, affecting around 2-3% of people over the age of 65. PD is characterized by intra-cellular aggregates of α-synuclein (syn) and neuron cell loss in the brain region of substantia nigra (SN), which results in deficiency in dopamine levels. Several other types of cell in the peripheral and central autonomic nerve are also involved, most probably from the beginning of the disease. PD is associated with numerous non-motor indicators that donate to overall infirmity, despite the fact a medical diagnosis of the ailment governed by the existence of bradykinesia and some of the other essential motor features. Several paths and machineries, containing proteostasis of syn, mitochondrial function, oxidative injuries, calcium homeostasis, axonal transport, and neuro-inflammation, are participated in the principal molecular pathogenesis. The mainstay of PD treatment is the pharmacological replacement of striatal dopamine. Non-dopaminergic methods are also utilized to treat non-motor and motor symptoms, and deep brain stimulation is utilized for patients who experience unmanageable motor complications related to L-DOPA. For the pharmacological treatment of PD, levodopa, dopamine agonists, monoamine oxidase inhibitors, and catechol-O-methyltransferase inhibitors are commonly used.