review · Frontiers in Pharmacology
Parkinson's disease is an age-related neurological disorder marked by movement difficulties and brain inflammation. Although non-steroidal anti-inflammatory drugs have shown neuroprotective effects in preclinical trials and animal models, human studies on their relationship with Parkinson's disease risk have historically produced conflicting results. To address this debate, a systematic review and meta-analysis evaluated data gathered from Scopus, PubMed, and Web of Science databases. Using random-effects statistical models, researchers measured the risk of developing Parkinson's disease among users of various pain-relieving medications. The findings reveal a statistically significant reduction in Parkinson's disease risk among individuals taking non-steroidal anti-inflammatories as a whole, non-aspirin anti-inflammatories, and ibuprofen specifically. Conversely, the analysis found that aspirin use was not associated with any significant change in the risk of developing the disease.
Parkinson's disease poses severe health challenges as populations age, with brain inflammation playing a recognised role in its pathology. By synthesising divergent clinical evidence, this analysis demonstrates that widely available anti-inflammatory drugs like ibuprofen correlate with reduced disease incidence. This helps clarify existing medical debates regarding preventative strategies and highlights potential neuroprotective pathways against neurodegenerative decline.
The findings could inform early-stage therapeutic repurposing and clinical prevention strategies explored by pharmaceutical developers and healthcare researchers targeting neurodegenerative diseases. However, because this research is a retrospective meta-analysis of existing observational data, any clinical or commercial application remains at an early stage and would require prospective clinical trials before guiding treatment protocols or preventative product developments.
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Background: Parkinson’s disease (PD) is a neurological condition that typically shows up with aging. It is characterized by generalized slowness of movement, resting tremor or stiffness, and bradykinesia. PD patients’ brains mostly exhibit an increase in inflammatory mediators and microglial response. Nevertheless, a variety of non-steroidal anti-inflammatory medications (NSAIDS) offered neuroprotection in animal models and preclinical trials. Aim: The current systematic review and meta-analysis were designed to try to resolve the debate over the association of NSAID use with the development of PD because the results of several studies were somehow contradictory. Methods: An intense search was performed on Scopus, PubMed, and Web of Science databases for articles relating the incidence of PD to the use of NSAIDs. Statistical analysis of the included studies was carried out using Review Manager version 5.4.1 by random effect model. The outcome was identified as the development of PD in patients who were on NSAIDs, ibuprofen only, aspirin only, and non-aspirin NSAIDs. This was analyzed using pooled analysis of odds ratio (OR) at a significance level of ≤0.05 and a confidence level of 95%. A statistically significant decreased risk of PD was observed in patients taking NSAIDs, Ibuprofen, and non-aspirin NSAIDs. Results: The ORs of PD occurrence in patients who took NSAIDs, Ibuprofen, and non-aspirin NSAIDs were 0.88 [95% CI (0.8–0.97), p = 0.01], 0.73 [95% CI (0.53–1), p = 0.05] and 0.85 [95% CI (0.75–0.97), p = 0.01]. Meanwhile, the risk of PD in patients who took aspirin was not statistically significant. Conclusion: In conclusion, Ibuprofen, non-aspirin NSAIDs, and other types of NSAIDs could be associated with a reduction in PD risk. However, there was no association between aspirin intake and the development of PD.
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DOI: 10.3389/fphar.2024.1434512
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