Welcome to DU!
The truly grassroots left-of-center political community where regular people, not algorithms, drive the discussions and set the standards.
Join the community:
Create a free account
Support DU (and get rid of ads!):
Become a Star Member
Latest Breaking News
General Discussion
The DU Lounge
All Forums
Issue Forums
Culture Forums
Alliance Forums
Region Forums
Support Forums
Help & Search
Do gut bacteria make a second home in our brains?
A few years ago there were a couple of studies examining whether Parkison's traveled from the gut via the vagus nerve to the brain.
Objective
Parkinson's disease (PD) may be caused by an enteric neurotropic pathogen entering the brain through the vagal nerve, a process that may take over 20 years. We investigated the risk of PD in patients who underwent vagotomy and hypothesized that truncal vagotomy is associated with a protective effect, whereas superselective vagotomy has a minor effect.
Methods
We constructed cohorts of all patients in Denmark who underwent vagotomy during 1977–1995 and a matched general population cohort by linking Danish registries. We used Cox regression to compute hazard ratios (HRs) for PD and corresponding 95% confidence intervals (CIs), adjusting for potential confounders.]
Interpretation
Full truncal vagotomy is associated with a decreased risk for subsequent PD, suggesting that the vagal nerve may be critically involved in the pathogenesis of PD. Ann Neurol
https://onlinelibrary.wiley.com/doi/abs/10.1002/ana.24448?fbclid=IwAR1bg5UsVjri4R0AR9aFrZbdiFpeddnmHh16dTF8cn_T1ddKtN7cAjy3fuc
Parkinson's disease (PD) may be caused by an enteric neurotropic pathogen entering the brain through the vagal nerve, a process that may take over 20 years. We investigated the risk of PD in patients who underwent vagotomy and hypothesized that truncal vagotomy is associated with a protective effect, whereas superselective vagotomy has a minor effect.
Methods
We constructed cohorts of all patients in Denmark who underwent vagotomy during 1977–1995 and a matched general population cohort by linking Danish registries. We used Cox regression to compute hazard ratios (HRs) for PD and corresponding 95% confidence intervals (CIs), adjusting for potential confounders.]
Interpretation
Full truncal vagotomy is associated with a decreased risk for subsequent PD, suggesting that the vagal nerve may be critically involved in the pathogenesis of PD. Ann Neurol
Per Borghammer's follow up papers: https://www.ncbi.nlm.nih.gov/pubmed/?term=Borghammer%20P&fbclid=IwAR1oMj-EQPY_Xtraomy06DUUbpYLbOjT9U6j2GLYmaG1QBYckyyHVaECj_Q
Compelling evidence .
At the annual meeting of the Society for Neuroscience, high-resolution microscope images were shown of bacteria apparently penetrating and inhabiting the cells of healthy human brains. The work is preliminary, and its authors are careful to note that their tissue samples, collected from cadavers, could have been contaminated. But to many passersby in the exhibit hall, the possibility that bacteria could directly influence processes in the brain—including, perhaps, the course of neurological disease—was exhilarating.
“This is the hit of the week,” said neuroscientist Ronald McGregor of the University of California, Los Angeles, who was not involved in the work. “It’s like a whole new molecular factory [in the brain] with its own needs. … This is mind-blowing.”
The brain is a protected environment, partially walled off from the contents of the bloodstream by a network of cells that surround its blood vessels. Bacteria and viruses that manage to penetrate this blood-brain barrier can cause life-threatening inflammation. Some research has suggested distant microbes—those living in our gut—might affect mood and behavior and even the risk of neurological disease, but by indirect means. For example, a disruption in the balance of gut microbiomes could increase the production of a rogue protein that may cause Parkinson’s disease if it travels up the nerve connecting the gut to the brain.
Talking hoarsely above the din of the exhibit hall on Tuesday evening, neuroanatomist Rosalinda Roberts of The University of Alabama in Birmingham (UAB), told attendees about a tentative finding that, if true, suggests an unexpectedly intimate relationship between microbes and the brain. Her lab looks for differences between healthy people and those with schizophrenia by examining slices of brain tissue preserved in the hours after death. About 5 years ago, neuroscientist Courtney Walker, then an undergraduate in Roberts’s lab, became fascinated by unidentified rod-shaped objects that showed up in finely detailed images of these slices, captured with an electron microscope. Roberts had seen the shapes before. “But I just dismissed them, because I was looking for something else,” she says. “I would say ‘Oh, here are those things again.’”
But Walker was persistent, and Roberts started to consult colleagues at UAB. This year, a bacteriologist gave her unexpected news: They were bacteria. Her team has now found bacteria somewhere in every brain they’ve checked—34 in all—about half of them healthy, and half from people with schizophrenia.
Roberts wondered whether bacteria from the gut could have leaked from blood vessels into the brain in the hours between a person’s death and the brain’s removal. So she looked at healthy mouse brains, which were preserved immediately after the mice were killed. More bacteria. Then she looked at the brains of germ-free mice, which are carefully raised to be devoid of microbial life. They were uniformly clean.
“This is the hit of the week,” said neuroscientist Ronald McGregor of the University of California, Los Angeles, who was not involved in the work. “It’s like a whole new molecular factory [in the brain] with its own needs. … This is mind-blowing.”
The brain is a protected environment, partially walled off from the contents of the bloodstream by a network of cells that surround its blood vessels. Bacteria and viruses that manage to penetrate this blood-brain barrier can cause life-threatening inflammation. Some research has suggested distant microbes—those living in our gut—might affect mood and behavior and even the risk of neurological disease, but by indirect means. For example, a disruption in the balance of gut microbiomes could increase the production of a rogue protein that may cause Parkinson’s disease if it travels up the nerve connecting the gut to the brain.
Talking hoarsely above the din of the exhibit hall on Tuesday evening, neuroanatomist Rosalinda Roberts of The University of Alabama in Birmingham (UAB), told attendees about a tentative finding that, if true, suggests an unexpectedly intimate relationship between microbes and the brain. Her lab looks for differences between healthy people and those with schizophrenia by examining slices of brain tissue preserved in the hours after death. About 5 years ago, neuroscientist Courtney Walker, then an undergraduate in Roberts’s lab, became fascinated by unidentified rod-shaped objects that showed up in finely detailed images of these slices, captured with an electron microscope. Roberts had seen the shapes before. “But I just dismissed them, because I was looking for something else,” she says. “I would say ‘Oh, here are those things again.’”
But Walker was persistent, and Roberts started to consult colleagues at UAB. This year, a bacteriologist gave her unexpected news: They were bacteria. Her team has now found bacteria somewhere in every brain they’ve checked—34 in all—about half of them healthy, and half from people with schizophrenia.
Roberts wondered whether bacteria from the gut could have leaked from blood vessels into the brain in the hours between a person’s death and the brain’s removal. So she looked at healthy mouse brains, which were preserved immediately after the mice were killed. More bacteria. Then she looked at the brains of germ-free mice, which are carefully raised to be devoid of microbial life. They were uniformly clean.
6 replies
= new reply since forum marked as read
= new reply since forum marked as read
