Parkinson’s Disease (PD) is characterized by resting tremor, slow movements, and rigid muscles. For decades we have known it involves dopamine-releasing neurons in the middle of the brain dying. However, in recent years scientists have suggested its origin could be in the gut rather than the brain.
For example, people with PD have been shown to experience symptoms in the gut, such as abnormal bacteria populations, and gut “leakiness”, which lets bacteria and toxins pass easily from the gut into the blood. Exactly how this relates to PD is a mystery.
In a paper published in Neurobiology of Disease in February, researchers used mice with PD-like features to investigate gut leakiness and fecal bacteria populations. Some of the mice were also chronically stressed, and the researchers compared their gut features to unstressed mice. The researchers examined their intestines under a microscope and measured their gut inflammation levels.
They found that the stressed mice had damaged, leaky intestines. Additionally, stress activated the microglia, small cells in the brain known for their role in inflammation and immunity. Chemical markers of inflammation were increased in these mice, and the types of bacteria found in their feces were also different than in unstressed mice: stress reduced the “anti-inflammatory” bacteria. Stressed mice with PD-like features had severe gut hyperpermeability.
This increase in gut inflammation could lead to increased inflammation in the brain too. These findings support the gut-brain axis hypothesis of PD, showing a role of chronic stress in driving this. Understanding what occurs in the gut, and what causes this gut disruption, would allow a whole new therapeutic strategy for treating PD.