The molecular processes involved in the development of Parkinson’s disease are not currently known. Emerging evidence suggests that inflammation plays a role in Parkinson’s pathogenesis. Research suggests a link between alpha-synuclein aggregates throughout the body and inflammatory processes linked with Parkinson’s disease. This link is supported by evidence that immune system activity drives neurodegeneration in Parkinson’s. Therefore, to study the link between controlling inflammation and Parkinson’s risk, patients with systemic inflammation should be studied because they can provide insight into the ability of anti-inflammatory treatment to modulate Parkinson’s risk.
In a retrospective study published in Parkinsonism and Related Disorders, researchers tracked the incidence of Parkinson’s in patients with autoimmune disorders who were being treated with anti-tumor necrosis factor (TNF) and anti-interleukin (IL)-17 drugs, both of which are systemic anti-inflammatory medications.
Patient data was sourced from the Komodo Health claims database, which includes deidentified records for 320 million people enrolled in US healthcare plans from 2012 to present. Patients had either in- or out-patient claims for rheumatoid arthritis (RA), ulcerative colitis (UC), Crohn’s disease (CD), ankylosing spondylitis (AS), or psoriasis/psoriatic arthritis (Ps/PsA). Patients were excluded if they had a Parkinson’s diagnosis at baseline. Patients with de-novo claims for use of anti-TNF therapies or IL-17 therapies were tracked and compared with auto-immune patients who do not take these anti-inflammatory medications. New incidence of Parkinson’s was tracked as the time-to-incidence of the first claim associated Parkinson’s treatment.
The data set included 2,105,677 patients with a confirmed diagnosis of RA, UC, CD, AS, or Ps/PsA; 114,082 received anti-TNF/anti-IL-17 treatment, 106,314 received anti-TNF only, 5672 received anti-IL-17 only, and 1,991,595 were untreated.
Incidence of Parkinson’s per 100 patient-years (PY) was 0.66 for the cohort treated with both an anti-TNF and anti-IL-17 vs 0.95 per PY in those who were untreated. The unadjusted incidence rate ratio (IRR) for exposed vs unexposed patients was 0.70 (95% CI: 0.70-0.72). For those treated with an anti-TNF only, the IRR was 0.67 (95% CI: 0.64–0.69), and for those treated with an anti-IL-17 only, the IRR was 0.52 (95% CI: 0.41–0.65). The IRR for those treated with an anti-IL-17 only vs an anti-TNF only was 0.78 (95% CI: 0.63-0.98).
An adjusted analysis that controlled for several covariates such as age, gender, and use of corticosteroids, non-steroidal inflammatory drugs, and other disease-modifying antirheumatic drugs found a significant risk reduction for those being treated with both anti-TNF/anti-IL-17 vs unexposed patients (adjusted IRR 0.77 [95 % CI: 0.74–0.80], P<0.0001). Results were similar for anti-TNF-only (adjusted IRR 0.77 [95 % CI: 0.74–0.81], P<0.0001) and anti-IL-17-only (adjusted IRR 0.64 [95 % CI: 0.52–0.80], P<0.0001) groups vs unexposed patients.
This retrospective cohort study highlights that anti-inflammatory drugs can reduce the risk of Parkinson’s disease, highlighting the link between inflammatory processes and Parkinson’s disease. Further studies will be needed to confirm the causal relationship of anti-inflammatory drugs and Parkinson’s disease.
