The exploration of the role of inflammation and its components and also the role of inflammation inhibition on neurodegenerative brain disorder Parkinsons disease (PD) were chosen as the base aim and interest of this review. PD is known to be a chronic/progressive neurodegenerative disease caused by a specific degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc) region of the striatum. A large number of experimental evidence indicates that the factors involved in the pathogenesis of this disease are several, occurring inside and outside the dopaminergic neuron. Recently, the role of the inflammatory process, in particular, has been the object of research interest by the scientific community. This assumes to represent a new therapeutic approach opportunity for this neurological disorder. Indeed, it has been demonstrated that the cyclooxygenase type 2 (COX-2) is over expressed in SNc Dopaminergic neurons in both PD patients and PD animal models and, furthermore, non-steroidal anti-inflammatory drugs (NSAIDs) and Steroidal anti-inflammatory drugs (SAIDs) pre-treatment protect against 1-methyl-4-phenyl-1, 2, 3, 6- tetrahydropyridine (MPTP) or 6 hydroxydopamine (6-OHDA)-induced nigrostriatal dopamine degeneration. Moreover, recent epidemiological studies have revealed that the risk of developing PD is reduced in humans who make therapeutical use of NSAIDs or SAIDs. Consequently, it is hypothesized that the onset of the disease might be delayed or prevented by the rational prescription of SAIDs or NSAIDs.