A story of the potential effect of non-steroidal anti-inflammatory drugs (NSAIDs) in Parkinson's disease: beneficial or detrimental effects

Parkinson's disease (PD) is an advanced neurodegenerative disease (NDD) caused by the degeneration of dopaminergic neurons (DNs) in the substantia nigra (SN). As PD is an age-related disorder, the majority of PD patients are associated with musculoskeletal disorders with prolonged use of analgesic and anti-inflammatory agents, such as non-steroidal anti-inflammatory drugs (NSAIDs). Therefore, NSAIDs can affect PD neuropathology in different ways. Thus, the objective of the present narrative review was to clarify the potential role of NSAIDs in PD according to the assorted view of preponderance. Inhibition of neuroinflammation and modulation of immune response by NSAIDs could be an effective way in preventing the development of NDD. NSAIDs affect PD neuropathology in different manners could be beneficial or detrimental effects. Inhibition of cyclooxygenase 2 (COX2) by NSAIDs may prevent the development of PD. NSAIDs afforded a neuroprotective role against the development and progression of PD neuropathology through the modulation of neuroinflammation. Though, NSAIDs may lead to neutral or harmful effects by inhibiting neuroprotective prostacyclin (PGI2) and accentuation of pro-inflammatory leukotrienes (LTs). In conclusion, there is still a potential conflict regarding the effect of NSAIDs on PD neuropathology.

Automated summary

Parkinson's disease (PD) is a degenerative disorder caused by the damage to certain neurons in the brain. The use of non-steroidal anti-inflammatory drugs (NSAIDs) to treat musculoskeletal problems in PD patients can have both beneficial and harmful effects on the progression of the disease. NSAIDs can potentially prevent the development of PD by reducing neuroinflammation, but they may also inhibit neuroprotective mechanisms and worsen neuroinflammation. In conclusion, the effect of NSAIDs on PD neuropathology is still uncertain and further research is needed.