New research conducted by Duke Health researchers suggests a link between gut health and the development of Parkinson’s disease. The study, which was published in the journal JCI Insight, sheds light on how a protein called alpha-synuclein (⍺-synuclein), found in the gut, travels through the nervous system and reaches susceptible nerves in the brain.
The study suggests that when ⍺-synuclein proteins become corrupted, they can spread from the gut to the brain, forming clumps known as Lewy bodies. Lewy bodies are the hallmark of Parkinson’s disease and other forms of dementia. This discovery supports the theory that Parkinson’s disease begins in the gut and then spreads to the brain.
Parkinson’s disease is a chronic degenerative disorder that affects voluntary movement. It is estimated that up to 10 million people worldwide are living with the disease. Previous studies have already indicated that the gut may play a role in the development of Parkinson’s disease. One key clue is that gastrointestinal symptoms, such as constipation, often occur before motor skills decline.
The researchers focused on specialized cells in the gut called enteroendocrine cells, which react to their environment and sense toxicants like herbicides and pesticides in the intestine. These cells also harbor ⍺-synuclein. Through experiments with cell cultures and mice, the researchers found that enteroendocrine cells transport ⍺-synuclein from gut mucosal cells to the brainstem via the vagus nerve, which is the body’s superhighway connecting the gut and brain.
Lead author Rodger Liddle, M.D., a professor in the Department of Medicine at Duke University School of Medicine, explained that when ⍺-synuclein becomes corrupted in the gut, it can misfold and cause issues with the transport system. Liddle stated, “We hypothesize that something in the gut is corrupting ⍺-synuclein, causing it to misfold. Whether this is toxicants or some other exposure, we don’t know. But we have demonstrated here that there is a route for pathologically misfolded ⍺-synuclein to be transported from enteroendocrine cells to the brain, where they can aggregate to form Lewy body deposits.”
The research team was able to disrupt the spread of ⍺-synuclein by severing the vagus nerve in the mice. This finding provides a foundation for developing therapies that could block the transport system or reset the altered gut-brain signaling.
Understanding the connection between gut health and Parkinson’s disease could lead to new strategies for early detection and treatment. This research opens doors for the potential development of interventions that target the gut to prevent the spread of corrupted ⍺-synuclein to the brain. Further studies and clinical trials will be needed to explore these possibilities and develop effective treatments for Parkinson’s disease.
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