Gut inflammation may initiate Parkinson’s disease, study finds

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In a new study from Van Andel Institute and Roche, researchers found that chronic inflammation in the gut may propel processes in the body that give rise to Parkinson’s disease.

The study is the latest in a growing list that links the gut and the immune system to Parkinson’s.

The researchers confirmed an association between Parkinson’s and inflammatory bowel diseases, such as ulcerative colitis and Crohn’s disease.

Epidemiological evidence from other groups indicates the risk of developing Parkinson’s fades in certain people whose inflammatory bowel disease is treated with anti-TNF, a standard-of-care anti-inflammatory therapy.

This suggests that reducing gut inflammation may have promise for delay Parkinson’s.

In the study, the team found that chronic gut inflammation triggers a protein called alpha-synuclein to clump together in walls of the colon, as well as in local immune cells called macrophages.

A similar process may play out in the colons of some people—such as those with inflammatory bowel diseases—thereby increasing their risk to develop Parkinson’s as shown in studies by other groups.

Similarly, in the brains of people with Parkinson’s, “sticky” alpha-synuclein aggregates also develop. For reasons that still are unclear, these aggregates can clog the molecular machinery that keep neurons alive.

The resulting loss of some of these critical cells—and the chemical messenger they produce called dopamine—causes Parkinson’s hallmark movement-related symptoms, such as freezing and loss of voluntary movement.

The additional wide-spread development of alpha-synuclein aggregates throughout the brain also may be associated with the disease’s non-motor symptoms and may fuel its progression, which cannot be slowed or stopped with existing treatments.

The study also found that chronic inflammation in the gut early in life can exacerbate alpha-synuclein clumping throughout the brain.

While it isn’t clear exactly how this happens, the team has two theories: first, they suggest inflammatory chemicals may travel from the gut to the brain via the bloodstream, triggering a runaway inflammatory immune response that leads to protein aggregation.

Another idea is that alpha-synuclein aggregates may travel to the brain via the vagus nerve, one of the longest nerves in the body and a “superhighway” between the gut and the brain. Once there, the proteins may then execute their toxic activity in the brain.

Notably, the team also found that a standard-of-care anti-inflammatory therapy for inflammatory bowel disease can help decrease the risk of developing Parkinson’s.

If you care about Parkinson’s disease, please read studies about these high blood pressure drugs may prevent dementia, Parkinson’s, Huntington’s and findings of coffee may help fight common dementia and Parkinson’s disease.

For more information about Parkinson’s disease prevention and treatment, please see recent studies about scientists discover roots of Parkinson’s in the brain and results showing that this mental problem may be linked to Parkinson’s disease.

The study is published in Free Neuropathology. One author of the study is Patrik Brundin, M.D., Ph.D.

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