If you are long in the tooth like me, you probably are. I hope that fear induces you to eat better. Get off refined foods, especially sugar and trans-fats. They disturb your immune system in the Microbiome (gut bacteria). Also eat as organic as possible.
Graduate work: become vegan.
References
SCFA and lipopolysaccharide as mediators between gut dysbiosis and amyloid pathology in Alzheimer’s Disease
J. Alzheimer’s Disease 2020;78:683
“Alzheimer’s disease is the most common cause of dementia. Still incurable, it directly affects nearly one million people in Europe, and indirectly millions of family members as well as society as a whole. In recent years, the scientific community has suspected that the gut microbiota plays a role in the development of the disease.
A team from the University of Geneva (UNIGE) and the University Hospitals of Geneva (HUG) in Switzerland, together with Italian colleagues from the National Research and Care Center for Alzheimer’s and Psychiatric Diseases Fatebenefratelli in Brescia, University of Naples and the IRCCS SDN Research Center in Naples, confirm the correlation, in humans, between an imbalance in the gut microbiota and the development of amyloid plaques in the brain, which are at the origin of the neurodegenerative disorders characteristic of Alzheimer’s disease. Proteins produced by certain intestinal bacteria, identified in the blood of patients, could indeed modify the interaction between the immune and the nervous systems and trigger the disease. These results, published in the Journal of Alzheimer’s Disease, make it possible to envisage new preventive strategies based on the modulation of the microbiota of people at risk.
The research laboratory of neurologist Giovanni Frisoni, director of the HUG Memory Centre and professor at the Department of Rehabilitation and Geriatrics of the UNIGE Faculty of Medicine, has been working for several years now on the potential influence of the gut microbiota on the brain, and more particularly on neurodegenerative diseases. “We have already shown that the gut microbiota composition in patients with Alzheimer’s disease was altered, compared to people who do not suffer from such disorders,” he explains. “Their microbiota has indeed a reduced microbial diversity, with an over-representation of certain bacteria and a strong decrease in other microbes. Furthermore, we have also discovered an association between an inflammatory phenomenon detected in the blood, certain intestinal bacteria and Alzheimer’s disease; hence the hypothesis that we wanted to test here: could inflammation in the blood be a mediator between the microbiota and the brain?”
The brain under influence
Intestinal bacteria can influence the functioning of the brain and promote neurodegeneration through several pathways: they can indeed influence the regulation of the immune system and, consequently, can modify the interaction between the immune system and the nervous system. Lipopolysaccharides, a protein located on the membrane of bacteria with pro-inflammatory properties, have been found in amyloid plaques and around vessels in the brains of people with Alzheimer’s disease. In addition, the intestinal microbiota produces metabolites—in particular some short-chain fatty acids—which, having neuroprotective and anti-inflammatory properties, directly or indirectly affect brain function.
“To determine whether inflammation mediators and bacterial metabolites constitute a link between the gut microbiota and amyloid pathology in Alzheimer’s disease, we studied a cohort of 89 people between 65 and 85 years of age. Some suffered from Alzheimer’s disease or other neurodegenerative diseases causing similar memory problems, while others did not have any memory problems,” reports Moira Marizzoni, a researcher at the Fatebenefratelli Center in Brescia and first author of this work. “Using PET imaging, we measured their amyloid deposition and then quantified the presence in their blood of various inflammation markers and proteins produced by intestinal bacteria, such as lipopolysaccharides and short-chain fatty acids.”
A very clear correlation
“Our results are indisputable: certain bacterial products of the intestinal microbiota are correlated with the quantity of amyloid plaques in the brain,” explains Moira Marizzoni. “Indeed, high blood levels of lipopolysaccharides and certain short-chain fatty acids (acetate and valerate) were associated with both large amyloid deposits in the brain. Conversely, high levels of another short-chain fatty acid, butyrate, were associated with less amyloid pathology.”
This work thus provides proof of an association between certain proteins of the gut microbiota and cerebral amyloidosis through a blood inflammatory phenomenon. Scientists will now work to identify specific bacteria, or a group of bacteria, involved in this phenomenon.
A strategy based on prevention
This discovery paves the way for potentially highly innovative protective strategies—through the administration of a bacterial cocktail, for example, or of pre-biotics to feed the “good” bacteria in our intestine. “However, we shouldn’t be too quick to rejoice,” says Frisoni. “Indeed, we must first identify the strains of the cocktail. Then, a neuroprotective effect could only be effective at a very early stage of the disease, with a view to prevention rather than therapy. However, early diagnosis is still one of the main challenges in the management of neurodegenerative diseases, as protocols must be developed to identify high-risk individuals and treat them well before the appearance of detectable symptoms.”
Multiple sclerosis: What role do gut microbes play?
www.medicalnewstoday.com/articles/319361. Maria Cohut, Ph.D.
“New research investigates the link between the microbial profile of the gut and the development of multiple sclerosis. While this link has been noted before, researchers now focus on the specific role played by some microbes in promoting this condition.
Share on PinterestPeople with MS have a specific microbial profile in the gut, but how do gut bacteria influence the progression of the disease?
An estimated 2.3 million people around the world are affected by multiple sclerosis (MS), which is an autoimmune disease characterized by a “misfiring” of the immune system – a process in which myelin, the insulation around nerves, is perceived as a “foreign body” and erroneously attacked.
Unfortunately, despite its high prevalence, little is known about what causes MS and there is currently no cure. Treatments are largely symptomatic, aimed at facilitating the management of the condition.
Previous research has pointed out that people diagnosed with MS have a specific gut microbial profile, showing that some bacteria are more abundant in the guts of people with MS while the levels of other bacteria are unusually low.
A new study from the University of California, San Francisco, led by Dr. Sergio Baranzini, went one step further and sought to investigate what the significance of some of those microbes is to the immune system.
Dr. Egle Cekanaviciute, another investigator involved with the study, explains that she and her colleagues were interested in going beyond just ascertaining an association.
“A lot of microbiome studies say, ‘These bacteria are increased in patients with a disease, and those bacteria are reduced.’ And then they stop. We wanted to know more: should we care about the ones that are increased because they are harmful or the ones that are decreased because perhaps they are helpful?”
Dr. Egle Cekanaviciute
The researchers’ findings are now published in the online issue of PNAS.
Gut microbiome ‘talks’ to immune system
As part of the study, the researchers analyzed the gut microbiomes of 71 people who had been diagnosed with MS. They did the same for 71 healthy people with no MS history (the controls).
After pinpointing which microbes were more present in the guts of people with MS, and which ones tended to be present to a lesser degree, the scientists used in vitro experiments to try to identify the specific roles of those microbes.
First, they tested whether these microbes could interact with human immune system cells to render them pro- or anti-inflammatory. The team noted that Akkermansia muciniphila and Acinetobacter calcoaceticus, which were commonly found in the guts of people with MS, prompted a pro-inflammatory response.
At the same time, Parabacteroides distasonis – which is found at abnormally low levels in the systems of people with an MS diagnosis – determined immune-regulatory responses.
Next, to try to understand the role that these bacteria play when interacting with the whole immune system, the researchers carried out tests in mice.
The results were similar: A. muciniphila and A. calcoaceticus stimulated an inflammatory response, while P. distasonis led to an anti-inflammatory effect.
From here, they wanted to see how an MS-specific gut microbiome in its totality might influence neurodegeneration. Using mice in which MS had been induced artificially, they performed fecal microbiota transplants and studied the effect of the microbe levels on the animals’ system.
It was found that the transplanted MS-specific microbiome led to the loss of important immune-regulatory cells. It also facilitated neurodegeneration, which, the team suggested, may point to a causal link between the gut microbiome and the development of MS.
The researchers told Medical News Today that, to their knowledge, this is the first study to look at the function of gut microbiota both in vitro and in vivo. Yet they acknowledge that they faced some limitations, including the restrictions of RNA sequencing, a technique they used to identify relevant bacteria.
“This is the first study in MS,” explained Dr. Baranzini, “that provides mechanistic (in vitro and in vivo) information on microbiota differences. One limitation is that the [RNA] sequencing is only at 16S resolution, thus we cannot identify every bacteria. Also, larger studies are needed to evaluate heterogeneity and eliminate confounders.”
Other important limitations that will need to be addressed in the future, the scientists explained for MNT, are to do with the specific interaction between gut bacteria and cells of the immune system.
As Dr. Cekanaviciute told us, “[A]lthough we have shown that immune cells respond to different bacteria by becoming either more pro-inflammatory or more regulatory, we don’t know exactly how the bacteria interact with the immune cells.”
