No Causal Link Between IBD, Parkinson’s in Large-scale Analysis

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by Steve Bryson, PhD |

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Parkinson's and IBD | Parkinson's News Today | DNA illustration

No causal relationship was identified between Parkinson’s disease and inflammatory bowel disease (IBD) or its major subtypes, Crohn’s disease and ulcerative colitis, in a large-scale European genetic analysis.

More research is needed to determine whether other types of intestinal inflammation or unknown inflammatory mediators contribute to developing Parkinson’s, the researchers noted.

The genetic analysis, “Association between inflammatory bowel disease and Parkinson’s disease: A Mendelian randomization study,” was published in Nature Parkinson’s Disease.

Evidence has suggested that chronic low-level intestinal inflammation may play a role in developing Parkinson’s disease, which is characterized by both motor and non-motor symptoms.

IBD, which includes Crohn’s disease (CD) and ulcerative colitis (UC), is marked by chronic intestinal inflammation. So far, several observational studies looking at an association between IBD and Parkinson’s have generated contradictory findings.

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Researchers at the University Hospital of Augsburg, Germany, applied a Mendelian randomization (MR) approach, which can identify a causative connection between the two diseases by detecting variations in genes that are randomly present from conception and therefore independent of factors that bias observational studies.

The team collected genetic data from genome-wide association studies (GWAS), wherein single changes in the genetic code, called single-nucleotide polymorphisms (SNPs), are compared between people with and without a condition to find genetic associations.

For Parkinson’s disease, this included 15 datasets that consisted of comparing 56,306 European Parkinson’s cases to 1.4 million healthy controls. For IBD, there were 7,045 clinically diagnosed cases and 456,327 controls.

To validate the results, a second IBD sample was used, consisting of 12,882 cases and 21,770 controls, as well as 5,956 diagnosed cases of Crohn’s disease and 14,927 controls, and 6,968 cases of ulcerative colitis with 20,464 controls.

To investigate the causal impact of IBD and Parkinson’s, 27 SNPs were selected. In the validation analyses, 62 SNPs were chosen for IBD, 52 for Crohn’s disease, and 37 for ulcerative colitis.

The analysis showed no evidence that genetically predicted IBD was associated with Parkinson’s disease. The validation analysis confirmed this result by showing no impact on IBD as a whole and Parkinson’s.

In addition, there was no evidence for a causal relationship between Crohn’s disease or ulcerative colitis, and Parkinson’s disease.

A secondary examination used a more recently developed method called CAUSE, which was designed to avoid false positives that may occur in other methods. Here, 2,688 SNPs were used for the primary analysis with IBD, and in the validation assessment, 2,125 SNPs for IBD, 2,111 for Crohn’s disease, and 2,136 for ulcerative colitis were applied.

Using CAUSE, no causal relationship was found between Parkinson’s and IBD, Crohn’s, or ulcerative colitis.

Although these findings contradict other studies that show an association between Parkinson’s and IBD, the researchers suggested that “[Parkinson’s disease] may not be directly caused by the diagnosis of IBD but rather by a related inflammatory mediator that is linked to [Parkinson’s disease] risk.”

“The present study suggests that neither IBD nor its subtypes CD and UC causally affect Parkinson’s disease in the European population,” the researchers wrote, “Further research is necessary to investigate whether intestinal inflammation impacts the development of [Parkinson’s disease].”