Summary: Researchers reveal patients with inflammatory bowel disease are 28% more likely to develop Parkinson’s disease. However, an anti-inflammatory treatment used to help those with IBD can significantly decrease the risk of developing the neurodegenerative disease.
Source: Mount Sinai Hospital.
A recent study from researchers at the Icahn School of Medicine at Mount Sinai provides new insights into a link between inflammatory bowel disease (IBD) and Parkinson’s disease, and may have significant implications for the treatment and prevention of Parkinson’s disease.
The recent study, published in JAMA Neurology, shows that individuals with IBD are at a 28% higher risk of developing Parkinson’s disease than those without IBD. However, if they are treated with anti-Tumor Necrosis Factor alpha (anti-TNFα) therapy, a monoclonal antibody that is commonly used to control inflammation in IBD patients, then their risk of developing Parkinson’s disease goes down significantly, and becomes even lower than that in the general population.
These new insights will allow for better screening of IBD patients for Parkinson’s disease, given that IBD onset usually precedes that of Parkinson’s disease by decades, and they also offer evidence to support exploring anti-TNFα therapy to prevent Parkinson’s disease in at-risk individuals.
While previous research had shown genetic and functional connections between IBD and Parkinson’s disease, clinical evidence linking the two has been scarce. The authors of the study previously identified a number of genetic variants that contributed to either an increased risk of both Parkinson’s disease and of Crohn’s disease, a type of IBD, or a decreased risk of both diseases, which prompted them to further study the co-occurrence of the two diseases.
“Systemic inflammation is a major component of IBD, and it’s also thought to contribute to the neuronal inflammation found in Parkinson’s disease,” explained Inga Peter, Professor in the Department of Genetics and Genomic Sciences at Mount Sinai and lead investigator in the study. “We wanted to determine if anti-TNFα therapy, could mitigate a patient’s risk in developing Parkinson’s disease.”
The Mount Sinai team found a 78% reduction in the incidence of Parkinson’s disease among IBD patients who were treated with anti-TNFα therapy when compared to those who were not.
It was previously thought that anti-TNFα therapies had limited effects on the central nervous system, the site where molecular mechanisms of Parkinson’s disease are found, because the large molecules in the anti-TNFα compounds cannot independently pass through the blood brain barrier. The outcomes of this study suggest that it may not be necessary for the drug to pass through the blood brain barrier to treat or prevent inflammation within the central nervous system, or that the blood-brain barrier in patients with IBD may be compromised, allowing the large molecules of the compound to pass through.
Parkinson’s disease ranks among the most common late-life neurodegenerative diseases, affecting approximately 1-2% of people 60 years or older. “Current therapies for Parkinson’s disease focus on ameliorating symptoms,” said Peter, “Our findings provide promising insights that support further investigations into how reducing systemic inflammation could help treat or prevent Parkinson’s disease.”
Source: Jennifer Gutierrez – Mount Sinai Hospital
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Original Research: Abstract for “Anti–Tumor Necrosis Factor Therapy and Incidence of Parkinson Disease Among Patients With Inflammatory Bowel Disease” by Inga Peter, PhD; Marla Dubinsky, MD; Susan Bressman, MD; Andrew Park, PhD, MPH; Changyue Lu, MS; Naijun Chen, MS; and Anthony Wang, PhD, MPH in JAMA Neurology. Published April 24 2018.
Control of mechanical pain hypersensitivity in mice through ligand-targeted photoablation of TrkB-positive sensory neurons
Importance Despite established genetic and pathophysiologic links between inflammatory bowel disease (IBD) and Parkinson disease (PD), clinical data supporting this association remain scarce. Although systemic inflammation is considered a potential biological mechanism shared between the 2 diseases, the role of reduced systemic inflammation through IBD-directed anti–tumor necrosis factor (anti-TNF) therapy in PD risk is largely unknown.
Objective To compare the incidence of PD among individuals with or without IBD and to assess whether PD risk among patients with IBD is altered by anti-TNF therapy.
Design, Setting, and Participants This is a retrospective cohort study analyzing information in the Truven Health MarketScan administrative claims database and the Medicare Supplemental Database between January 1, 2000, and March 31, 2016. Individuals were selected who had at least 2 claims for IBD diagnoses, at least 6 months of follow-up, and no prior diagnosis of PD on or before the IBD index date. Exposure to Anti-TNF therapy was measured from the anti-TNF index date to the last date of anti-TNF coverage or the end of enrollment or PD index date, whichever was earliest. Incidence rates per 1000 person-years were calculated, and crude and adjusted incidence rate ratios were estimated by Poisson regression models and presented with 95% CIs.
Main Outcomes and Measures Incidence of PD among patients with IBD with or without exposure to anti-TNF therapy.
Results In total, 144 018 individuals with IBD were matched on age, sex, and year of index date with 720 090 unaffected controls. Of them, 1796 individuals had at least 2 PD diagnoses and at least 1 filled PD-related prescription. The mean (SD) age of individuals with IBD was 51 (17) years, and 44% were men. The incidence of PD among patients with IBD was 28% higher than that among unaffected matched controls (adjusted incidence rate ratio, 1.28; 95% CI, 1.14-1.44; P < .001). A 78% reduction in the incidence rate of PD was detected among patients with IBD who were exposed to anti-TNF therapy compared with those who were not exposed (adjusted incidence rate ratio, 0.22; 95% CI, 0.05-0.88; P = .03).
Conclusions and Relevance A higher incidence of PD was observed among patients with IBD than among individuals without IBD. Early exposure to antiinflammatory anti-TNF therapy was associated with substantially reduced PD incidence. These findings support a role of systemic inflammation in the pathogenesis of both diseases. Further studies are required to determine whether anti-TNF treatment administered to high-risk individuals may mitigate PD risk.