What if doctors could change your diet and reduce the chances of developing multiple sclerosis?
That’s what Brigham and Women’s researchers are suggesting, after discovering that the bacteria living in the gut and the way it processes certain foods can control inflammation and neurodegeneration.
“What you eat can affect preexisting conditions,” said corresponding author Francisco Quintana, an investigator in the Ann Romney Center for Neurologic Diseases at Brigham and Women's Hospital. “At least in this moment, the data we have now, is what you eat and how that is processed by the bacteria you have in your gut affects ongoing inflammation in the brain.”
The finding, published today in the journal Nature Medicine, is presenting researchers with new potential therapies for MS, and may also be relevant to managing or controlling other brain diseases.
Quintana and investigators wanted to explore the suggested connection between the brain and the gut, and so analyzed the star-shaped cells in the brain and spinal cord of mice with multiple sclerosis, called astrocytes.
What scientists discovered was a molecular pathway involving inflammation. When bacteria in the gut broke down tryptophan, an amino acid famously found in turkey, it released a molecule that influenced this pathway. When more of these molecules were present, the brain and spinal cord cells were able to limit inflammation in the brain.
The phenomenon was also present in humans. Patients with MS had decreased levels of these tryptophan-derived molecules.
Quintana said researchers may identify supplements to produce more of this molecule in patients that lack it, or are looking at probiotics that can boost anti-inflammatory pathways.
"humans with MS to see if changes in diet or bacteria do produce an immune response. Researchers are also hopeful about exploring the role food may play in other cognitive roles, such as memory.
“The take-home message, you can think of it like a remote control,” Quintana said. “You have gut bacteria controlling your brain.”
http://www.bizjournals.com/boston/bl...-a-remote.html
That’s what Brigham and Women’s researchers are suggesting, after discovering that the bacteria living in the gut and the way it processes certain foods can control inflammation and neurodegeneration.
“What you eat can affect preexisting conditions,” said corresponding author Francisco Quintana, an investigator in the Ann Romney Center for Neurologic Diseases at Brigham and Women's Hospital. “At least in this moment, the data we have now, is what you eat and how that is processed by the bacteria you have in your gut affects ongoing inflammation in the brain.”
The finding, published today in the journal Nature Medicine, is presenting researchers with new potential therapies for MS, and may also be relevant to managing or controlling other brain diseases.
Quintana and investigators wanted to explore the suggested connection between the brain and the gut, and so analyzed the star-shaped cells in the brain and spinal cord of mice with multiple sclerosis, called astrocytes.
What scientists discovered was a molecular pathway involving inflammation. When bacteria in the gut broke down tryptophan, an amino acid famously found in turkey, it released a molecule that influenced this pathway. When more of these molecules were present, the brain and spinal cord cells were able to limit inflammation in the brain.
The phenomenon was also present in humans. Patients with MS had decreased levels of these tryptophan-derived molecules.
Quintana said researchers may identify supplements to produce more of this molecule in patients that lack it, or are looking at probiotics that can boost anti-inflammatory pathways.
"humans with MS to see if changes in diet or bacteria do produce an immune response. Researchers are also hopeful about exploring the role food may play in other cognitive roles, such as memory.
“The take-home message, you can think of it like a remote control,” Quintana said. “You have gut bacteria controlling your brain.”
http://www.bizjournals.com/boston/bl...-a-remote.html
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