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Study shows brain treatment may temper Crohn’s disease


Winnipeg, MB – Recent data from the Inflammatory Bowel Disease (IBD)-Clinical and Research Centre at the University of Manitoba in Winnipeg have demonstrated that those with inflammatory bowel disease are more likely to have a mood disorder long before their disease diagnosis compared to unaffected controls in the general population.

“This raises the possibility that brain disorders may predispose individuals to gut disorders; other evidence supports the important interrelationship between psychiatric disorders and inflammatory bowel disease,” said Dr. Jean-Eric Ghia, assistant professor, Faculty of Health Sciences, University of Manitoba and principal investigator in a study published today in the on-line edition of PLOS ONE.

 “Moreover, over the last 10 years, it has been demonstrated in animal models of IBD that an important nerve connecting the brain to gut, the vagus nerve, is altered. That nerve originates in the brain and extends to the gastrointestinal tract.”

Five years ago, Canadian research led by Dr. Stephen Collins and Ghia at McMaster University in Hamilton, Ontario demonstrated a deleterious effect of the absence of the vagus nerve in experimental models of IBD.

Recently, Ghia’s group reported that the central activation of the vagus nerve inhibits acute inflammation in mice models of colitis resembling Crohn’s disease. Treatments with galantamine, a drug used to treat Alzheimer’s disease, improved the acute colitis through a specific type of immune cell. However, the anatomical pathway was yet to be determined.

New research conducted by scientists in Ghia’s laboratory in the University of Manitoba, College of Medicine’s Departments of Immunology and Internal Medicine, Section of Gastroenterology suggests it is highly likely, that in mice, this nerve can be stimulated from the brain by activating a specific type of muscarinic one (M1) receptor to decrease the inflammatory process in the gut.

First author Peris Munyaka, a PhD student under Ghia, and her colleagues evaluated mice, which had their vagus nerves, and indirectly their splenic nerves and the spleen stimulated with a specific central M1 agent representing a class of drug currently under clinical trials to treat Alzheimer’s disease.

“First we demonstrated that this agent, by modifying something in the brain, can significantly decrease gut inflammation. Secondly, in the absence of the vagus nerve, splenic nerve or spleen, the beneficial effect of the central treatment is abolished, suggesting that, in this context, these three key actors may be the links between the brain and colonic inflammation,” said Ghia.