Six gut chemicals could flag dementia years before diagnosis

 

You need this testing post stroke so your competent? doctor can initiate dementia prevention protocols! Your doctor doesn't have them? Tough luck, you were handed an incompetent doctor!

Send me hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and title(If you can't stand by your name don't bother replying anonymously) and my response in my blog. Or are you afraid to engage with my stroke-addled mind? I would like to know why you haven't created dementia prevention protocols, and what is your definition of competence in stroke? Swearing at me is allowed, I'll return the favor.

With your chances of getting dementia post stroke, your competent? doctor needs to be monitoring this and provide dementia prevention solutions. Over a decade to accomplish that! Was it done? NO? So, you DON'T have a functioning stroke doctor, do you? YOUR DOCTOR IS RESPONSIBLE FOR PREVENTING THIS!

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here:

Six gut chemicals could flag dementia years before diagnosis

Lots of research suggests that healthy hearts lower our risk of dementia. 

But it seems gut changes might matter, too. 

Dr David Vauzour, lead researcher of the paper published in Gut Microbes, said: “Even in people who had only just begun noticing mild memory changes, there were clear shifts in both their gut bacteria and the metabolites they release into the bloodstream”. 

What might gut changes say about dementia risk?

The researchers looked at stool samples from 150 adults aged 50 and over. Some were healthy, while others had mild cognitive impairment (MCI), sometimes seen as a precursor to dementia.

There was also a third group of people who performed normally on cognitive tests but who said they felt like something “wasn’t quite right” with their memory or cognition.

All participants gave the researchers both fasting blood samples (which were used to identify 33 key molecules made in our gut) and stool samples (used to identify the gut bacteria of participants). 

“We explored whether specific combinations of these gut and diet-derived chemicals could separate the healthy from those experiencing early cognitive decline,” Dr Vazour said. 

“What we found was really striking. Even in people who had only just begun noticing mild memory changes, there were clear shifts in both their gut bacteria and the metabolites they release into the bloodstream.”

They built a machine-learning model on just six of these metabolites. It was able to classify people into the three groups with 79% accuracy, and could tell cognitively healthy adults apart from those with mild cognitive impairment with over 80% accuracy.

The chemical changes seen in participants’ blood samples seemed to be linked to the bacteria present (or absent) in their stool, which Dr Vaxour said adds “weight to growing evidence that the so‑called gut–brain axis ― the communication network between our digestive system and the brain ― may play an important role in cognitive ageing”. 

Researchers hope to use these findings to build a diagnostic tool

The study’s co-author, Dr Simon McArthur from Queen Mary University of London, has high hopes for the findings. 

“While we’re not yet at the point of providing a diagnostic test, our work suggests we may be able to use dietary and microbial information to help catch the presence of dementia earlier in life, potentially even before significant brain damage has occurred,” he said.

“We hope this work will pave the way for simple, non-invasive blood tests capable of identifying people at higher risk of memory decline years before dementia is typically diagnosed.” 

For his part, Dr Vauzor added, “If particular gut bacteria or the chemicals they produce contribute to early cognitive decline, treatments involving diet, probiotics, microbiome‑based therapies, or personalised nutrition could one day form part of dementia prevention strategies.” However, writing for the Science Media Centre, Prof Eef Hogervorst, a Professor of Biological Psychology at Loughborough University, wasn’t as convinced.

He said, “It is an interesting finding and a very well-written paper with good theory and impressive statistical analyses, but with small groups and no follow-up, I think the conclusion that this can be an early diagnostic marker for cognitive decline and even dementia may be a little overstated.” 

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Six Gut Markers May Identify Early Cognitive Decline

 Will your competent? doctor test for these AND CREATE DIET PROTOCOLS to have the correct gut bacteria/microbiota?

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!

Six Gut Markers May Identify Early Cognitive Decline

Key Takeaways

• Six diet- and gut-derived metabolites identified early cognitive impairment in older adults in a small study.
• The metabolite panel distinguished healthy controls from those with mild or subjective cognitive impairment.
• Findings suggest that metabolic disruptions may occur before clinical symptoms of dementia.

Six blood metabolites produced by or associated with gut microbiota identified early cognitive impairment in a small study.

The circulatory metabolites -- 5-hydroxyindole acetic acid, indole-3-propionic acid, choline, indoxyl sulfate, kynurenic acid, and kynurenine -- distinguished cognitively healthy older adults from those with mild cognitive impairment with an area under the curve (AUC) of 0.79, reported David Vauzour, PhD, of the University of East Anglia in Norwich, England, and co-authors.

The metabolites also separated healthy controls from people with subjective cognitive impairment with an AUC of 0.75, Vauzour and colleagues wrote in Gut Microbes.

"This study shows that a small set of gut‑ and diet‑derived blood metabolites can reliably distinguish healthy aging from early cognitive decline, even at the very earliest stage," Vauzour told MedPage Today.

The panel of six metabolites reflects early metabolic disruption along the gut-brain axis, he noted. "These results highlight that metabolic alterations appear long before cognitive decline is clinically apparent, offering a non‑invasive and scalable approach for early risk identification," Vauzour said.

"Because circulating metabolites integrate both gut microbial activity and host physiology, they outperform microbiome‑only metrics and offer promising avenues for early detection, monitoring, and targeted intervention strategies," he added.

Recent research showed that the composition of the gut microbiome correlated with amyloid and tau markers in people with asymptomatic Alzheimer's disease. Growing evidence also suggests that changes to gut bacteria may be linked to dementia risk, noted Sheona Scales, PhD, of Alzheimer's Research UK, which supported the study.

"While current blood tests for Alzheimer's work by detecting levels of specific proteins linked with the disease, this research may offer a new avenue for future blood test development," Scales wrote on the U.K. Science Media Centre website.

"This study can't say whether people with early memory and thinking problems will go on to develop dementia, but it identifies an interesting area for further research," she pointed out. "Given the study involved a relatively small group of people, larger and longer-term studies are needed to build on these findings and understand whether this type of test could be used alongside existing ones."

Vauzour and co-authors studied 150 older adults: 50 cognitively healthy controls, 50 participants with subjective cognitive impairment, and 50 with objectively measured mild cognitive impairment.

Groups were matched on age, sex, and body mass index. The mean age across groups was 65.5 years and 54% were women. Blood and fecal sample data came from baseline measurements of two previously conducted clinical studies.

Participants were excluded if they had a history of significant neurologic, psychiatric, gastrointestinal, or metabolic disorders; chronic fatigue syndrome; or gallbladder abnormalities. Additional exclusion criteria included current or recent smoking, alcohol or drug dependency, and clinically significant depression or anxiety. Individuals were ineligible if they were taking antidepressants, antipsychotics, anticoagulants, or any medications affecting gastrointestinal function.

Mass spectrometry platforms analyzed 33 metabolites in serum -- 13 tryptophan-related compounds, 15 bile acid compounds, three trimethylamine N-oxide-related metabolites, and two cresol metabolites. Microbiome analysis using 16S rRNA amplicon sequencing was used to detect bacterial taxa associated with metabolic changes.

The researchers used multiple linear regression and machine learning techniques to identify a metabolite panel capable of classifying early cognitive decline. Of the six metabolites in the panel, all except choline were products of tryptophan metabolism.

"The work underscores tryptophan metabolism as a key pathway disrupted early in cognitive decline, with protective metabolites decreasing and inflammatory or toxic metabolites increasing," Vauzour said. "The observation that biological changes arise at the subjective cognitive impairment stage further supports the need to shift prevention efforts earlier in the disease trajectory."

While the study adjusted for key covariates, metabolome profiles can be influenced by a plethora of environmental and biological factors, the researchers acknowledged. Metabolite changes may reflect physiological states associated with systemic inflammation, for example. "Thus, although our findings suggest relationships between the variables, we cannot infer causal relationships from this analysis alone," they wrote.

Future work should validate these metabolite signatures in larger, independent cohorts and across more diverse populations, Vauzour suggested.

"Longitudinal studies are needed to determine whether these metabolic changes can predict conversion from subjective cognitive impairment to objective cognitive impairment, and eventually, dementia," he stated. "Mechanistic studies, including microbiome manipulation or dietary interventions, could help clarify causal pathways and support the development of personalized, metabolite‑guided prevention strategies."

Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Connect:

Disclosures

The microbiota analysis in this study was supported by an Alzheimer's Research UK Small Pump Priming Grant.

Vauzour and co-authors reported no competing interests.

Scales had no disclosures.

Primary Source

Gut Microbes

Source Reference: Connell E, et al "Circulatory dietary and gut-derived metabolites predict early cognitive decline" Gut Microbes 2026; DOI: 10.1080/19490976.2026.2649487.

How Gut Bacteria Could Trigger Memory Loss as We Age

 Will your competent? doctor ensure this problem doesn't add onto your memory problems post stroke? Do you have a functioning stroke doctor, or not?

How Gut Bacteria Could Trigger Memory Loss as We Age

Memory loss and aging go hand-in-hand for most of us, but scientists are getting closer to understanding why. A new study, conducted by researchers at the Arc Institute in Palo Alto, California, and published in Nature, found that a prime suspect may be living in our gut.

“The biggest question that came out of this experiment is: How does the brain know about what’s going on [in the microbiome]?” said Christoph Thaiss, PhD, core investigator at Arc Institute and an assistant professor of pathology at Stanford University, Stanford, California. 

Thaiss focuses his research on how environmental factors, as well as age, predispose individuals to various diseases over the course of their life. When he teamed up with first author Timothy Cox, MD/PhD student at the University of Pennsylvania, Philadelphia, he’d set his sights on the aging gut microbiome. 

The Perfect Test Subjects

“It was previously known that the microbiome changes with age in the same way that we, the host, change with age,” explained Cox. “And so the question was, are there any consequences of that?”

To answer, the researchers took a group of old and young mice and had them live together. When mice cohabitate, “their microbiomes kind of average out because the mice are coprophagic,” said Cox. 

In other words, they eat each other’s poop.

The researchers were surprised by what they observed. After just a month, the young mice that were “otherwise totally healthy” showed signs of severe memory impairment.

Cox had extensive experience conducting memory tests on mice from his previous research on Alzheimer’s disease. “The main test that we use is something called novel object recognition. This takes advantage of the fact that mice are naturally curious and they like to explore new things,” said Cox.

Researchers show mice two identical objects, and the mice get to explore those objects so they learn what they are. Then they remove those objects. An hour later, they put the familiar object back in the cage “along with a new object called the novel object,” said Cox.

Normal mice remember that they’ve seen the familiar object and will spend 2-3 times more time exploring the novel object because it’s new and interesting to them. “Old mice, mice with Alzheimer’s disease, or those that have cognitive impairment forget that they’ve seen the first object before,” said Cox. “When they get exposed to the two objects for the testing phase, instead of spending more time with the new object, they spend equal time with both objects.”

A Surprising Result

The research team was not expecting to see any memory impairment in the young mice, let alone severe memory impairment. “But when we tested the young mice that were living with old mice, they were basically identical to the old mice in terms of performance. They did really poorly on the standard test,” said Cox.

The team was in such disbelief, in fact, that they had multiple people repeat the test to see if they could get the same outcome. “The more experiments we did, the more we got the same thing, and so we became more and more confident in it,” said Cox.

While the research team was surprised by the results, David Hafler, MD, professor of immunobiology and former chairman of the Department of Neurology at Yale School of Medicine, New Haven, Connecticut, was not. “I wasn’t surprised, but I was really very delighted to see more evidence of the gut-brain [connection],” he said (he was not involved in the study).

How This Gut-Brain Connection Works

To find a possible culprit in the gut, the team used germ-free mice. They transplanted the microbiomes of healthy, young mice and old mice and observed the exact same effects: The germ-free mice that received the old microbiomes displayed learning and memory impairment. “This gave us really strong evidence that this was a microbiome phenotype because it was reproduced with a fecal transplant,” said Cox. 

After testing several, they narrowed the search down to a bacterium called Parabacteroides goldsteinii, though Thaiss believes “there are other species that change with age, and there might be other species that have cognitive impact.”

The main function of P goldsteinii is its production of medium-chain fatty acids (MCFAs). High levels of MCFAs accumulate with age and activate gut-resident myeloid immune cells to produce inflammatory signaling molecules. This study allowed researchers to dive into the gut-brain connection, tracing the effects of MCFAs through intestinal immune cells into sensory neurons and up the vagus nerve into the hippocampus of the brain, where memories are formed. The result: “The function of vagal afferent neurons is impaired, the interoceptive signal received by the brain is weakened, and hippocampal function declines,” they write.

“It all fits in with these bigger narratives,” said Hafler. “This is all in mice, and our work has been in both mice and humans, but I think it’s really exciting and suggests the importance of these pathways. I think it just adds to the story of the increasing importance of the gut-brain connection. It’s just becoming increasingly clear.”

Next Steps

A deeper understanding of the gut’s role in cognitive decline could have implications beyond memory impairment. “We did several methods of vagal nerve stimulation. We’re able to restore memory in mice,” said Cox. “Vagal nerve stimulation is already FDA-approved for epilepsy and depression, but it’s now being looked at for many different diseases, including rheumatoid arthritis, inflammatory bowel disease, and multiple sclerosis. In the future, we might be able to apply that to cognitive decline.”

“Ultimately, the goal is to do something about cognitive decline in humans,” said Thaiss. “How can we understand and manipulate this communication [between the gut and the brain]? How much of this pathway is active and involved in regulating cognitive decline in humans? These are the two main questions that have come out of this study that I think are going to keep us and others in the field busy for a while.”

David Hafler declared having no competing interests. Disclosure information for all study authors is available in the original study publication.

Intense Exercise May Alter Gut Bacteria Composition, Study Finds

 Have your competent? doctor determine the EXACT LEVEL OF EXERCISE so as not to destroy the beneficial effects already provided by your DOCTORS' EXACT DIET PROTOCOL!  Oh, you don't have a diet protocol, do you? So, your doctor has already proven incompetence and you can't expect anything better than the crapola you already received!

Intense Exercise May Alter Gut Bacteria Composition, Study Finds

Scientists discover how to turn gut bacteria into anti-aging factories

 

Do you have ANY CONFIDENCE AT ALL that your stroke medical 'professionals' will get human testing going?

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!

Scientists discover how to turn gut bacteria into anti-aging factories

Date:

February 1, 2026

Source:

Howard Hughes Medical Institute

Summary:

Researchers found that small doses of an antibiotic can coax gut bacteria into producing a life-extending compound. In worms, this led to longer lifespans, while mice showed healthier cholesterol and insulin changes. Because the drug stays in the gut, it avoids toxic side effects. The study points to a new way of promoting health by targeting microbes rather than the body itself.

Scientists discovered that gently tweaking gut bacteria with a low-dose antibiotic can spark the production of compounds linked to longer life. The strategy improved lifespan and metabolic health in animals without harmful side effects. Credit: Shutterstock

Researchers have discovered a way to coax the bacteria living in animals' digestive systems into acting like miniature factories that produce compounds linked to longer life. The findings point to a potential new approach for developing drugs that work by influencing gut microbes rather than directly targeting the body.

The work was led by Janelia Senior Group Leader Meng Wang, whose lab focuses on understanding the biology of aging. Her team wanted to find a practical way to translate their earlier discoveries about longevity-related compounds into something that could eventually be useful beyond the laboratory.

Using the Gut Microbiota to Produce Beneficial Compounds

The researchers explored whether they could prompt the body's gut microbiota (a collection of bacteria in the gut that produces many different compounds) to make substances that support health and longevity. They focused on colanic acid, a compound naturally produced by gut bacteria that had already been shown to extend lifespan in roundworms and fruit flies.

In their latest experiments, Wang's team found that gut bacteria produced much higher levels of colanic acids when exposed to low doses of the antibiotic cephaloridine. Roundworms given cephaloridine lived longer, linking the increase in this bacterial compound to improved longevity.

The researchers then tested the approach in mice. Low doses of cephaloridine activated gene expression in gut bacteria involved in making colanic acids. This led to noticeable shifts in age-related metabolism, including higher levels of good cholesterol and lower levels of bad cholesterol in male mice, along with reduced insulin levels in female mice.

Why the Approach Avoids Side Effects

Cephaloridine has an important advantage. When taken orally, it is not absorbed into the bloodstream. That means it can influence the gut microbiome without affecting the rest of the body, helping to avoid toxicity and unwanted side effects.

According to the researchers, the results highlight a promising strategy for promoting longevity using drugs that act on bacteria rather than human cells. They suggest this work could reshape how future medicines are designed, shifting the focus toward compounds that guide the microbiota to produce health-supporting molecules for their hosts.

Journal Reference:

1. Guo Hu, Marzia Savini, Matthew Brandon Cooke, Xin Wei, Dinghuan Deng, Shihong M. Gao, Ruyue Alps Xia, Youchen Guan, Alice X. Wen, Xin Yu, Jin Wang, Chao Jiang, Christophe Herman, Jiefu Li, Meng C. Wang. Chemical modulation of gut bacterial metabolism induces colanic acid and extends the lifespan of nematode and mammalian hosts. PLOS Biology, 2025; 23 (11): e3002749 DOI: 10.1371/journal.pbio.3002749

• RELATED TOPICS
  • Health & Medicine
    • Cholesterol
    • Healthy Aging
    • Gastrointestinal Problems
    • 
      

Study identifies link between gut bacteria and deterioration of the brain in ALS, dementia

Will your incompetent? doctor and hospital ensure research occurs that IDENTIFIES AN EXACT PROTOCOL to prevent this deterioration?

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!

 Study identifies link between gut bacteria and deterioration of the brain in ALS, dementia

A significant discovery by Case Western Reserve University researchers could change how doctors treat two of the most devastating neurodegenerative diseases.

The team identified a link between gut bacteria and the deterioration of the brain in Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD). The researchers discovered that certain bacterial sugars cause immune responses that kill cells-and how to prevent it.

FTD mainly affects the brain's frontal and temporal lobes, causing changes in a person's personality, behavior and language. ALS primarily targets motor neurons, resulting in gradual muscle weakness and paralysis.

Most causes of ALS and FTD cases are unknown, although researchers have been examining several potential reasons, including genetics, environmental issues, brain injuries and diet.

The study, recently published in Cell Reports, solves a long-standing question about neurodegenerative diseases. The team discovered a molecular connection that explains why some people with specific genetic mutations acquire FTD and ALS and others don't.

We found that harmful gut bacteria produce inflammatory forms of glycogen (a type of sugar), and that these bacterial sugars trigger immune responses that damage the brain."

Aaron Burberry, assistant professor, Department of Pathology, Case Western Reserve School of Medicine

Burberry, the study's senior investigator, reported that 70% of the 23 ALS/FTD patients examined had dangerous glycogen levels. Of those without the brain diseases, only a third had high levels of glycogen.

The study has immediate implications for patient care by identifying new targets to treat ALS and FTD, while providing biomarkers to identify patients who might benefit from gut-targeted therapies.

Healing the gut can reduce long-term impact of stroke

 Is your competent? doctor and hospital ensuring this research gets completed and a protocol created? NO? So, you don't have a functioning stroke doctor or hospital? Why are you staying at an incompetent place?

Healing the gut can reduce long-term impact of stroke

A paper published this fall by researchers in the Department of Neuroscience and Experimental Therapeutics at the Texas A&M College of Medicine is the latest of multiple studies highlighting the potential of this novel avenue of treatment, which takes advantage of the link between the brain and digestive system to curb cognitive impairment and other lingering impacts of a stroke or brain trauma.

The team demonstrated how a drug that was effective at protecting the brain in the immediate aftermath of a stroke failed to prevent long-term cognitive impairment when applied only to the brain. The same drug, when applied to the gut, reduced impairment significantly.

"Just fixing the brain directly won't do it. As a neuroscientist, that was kind of shocking to me," said Regents Professor and Department Head Dr. Farida Sohrabji. "But this tells us that if you don't repair the gut, you won't see (improvement in long-term function)."

The study, which appears in the November edition of Brain, Behavior, and Immunity, builds on previous research led by Sohrabji, spearheaded by graduate student Yumna El-Hakim and associate research scientist Dr. Kathiresh Kumar Mani, exploring how the brain and gut influence each other during and after a stroke. By understanding and leveraging the relationship between these systems, the team hopes to develop therapeutic techniques to prevent cognitive impairment in stroke patients and reduce their risk of developing dementia or Alzheimer's disease (AD). Their work is supported by a grant awarded to Sohrabji by the National Institutes of Health, as well as additional funding from the WoodNext Foundation.

"Stroke is one of the leading causes of dementia and AD," Sohrabji said. "While there are acute, immediate consequences of stroke, there are also these long-term consequences that affect quality of life for the patient as well as the caregivers, so there's a lot of interest in understanding how to improve long-term outcomes."

What Happens In The Gut After A Stroke?

Within mere moments of a stroke, patients experience a cascade of symptoms, many of which are immediately apparent, Sohrabji said.

"You have individuals who can't lift their arms, whose faces droop on one side, their speech is slurred," she said. "That's classic and occurs very, very quickly."

Less apparent, she said, is the damage being done to key structures in the intestine, as the brain communicates to the gut that something is wrong. "What we've found is that minutes after a stroke occurs, normal gut anatomy is completely disrupted," Sohrabji explained.

Most notably, cells responsible for keeping the contents of the gut sealed off from the rest of the body begin to erode, allowing digestive bacteria to leak out and cause harm to other bodily systems. Under certain conditions, Sohrabji said, these bacteria can end up in the brain itself and disrupt its functioning. Even if bacteria don't make it all the way to the brain, brain function can still be impaired as the body's immune system recognizes the threat and mounts an inflammatory response to fight it. Increased inflammation exacerbates the impact of a stroke, further injuring the brain and increasing long-term cognitive impairment.

"If you just repair the brain, you will see short-term effects but not long-term improvement because the gut is still leaky," Sohrabji said. "It's (causing inflammation) and constantly impacting brain function in the long term."

Heal The Gut, Save The Brain

In the 2024 study, a treatment applied directly to the gut -- a dose of Insulin-like Growth Factor or IGF-1 -- was shown to significantly reduce post-stroke inflammation and cognitive impairment. Sohrabji and her team's investigation showed that the structures in the gut that become damaged after a stroke appeared to be repaired by the IGF-1 treatment, reinforcing the idea that healing the gut is crucial in facilitating stroke recovery.

In addition to its recent work with IGF-1, the team is exploring the use of stem cell transplants to rapidly repair the gut after a stroke -- a treatment proposed by Mani that has proven effective in previous studies.

Under normal conditions, the gut produces a steady supply of stem cells to repair itself, Sohrabji said. Existing research shows that these cells can be transplanted from a healthy donor to a host with a damaged gut to speed up their recovery.

"We were fairly sure that (the stem cells) would repair the gut. What was not known, and what was a very pleasant surprise to us, was that in that process, it also improved stroke outcomes," Sohrabji said. "As a result of (the treatment), the amount of dead tissue in the brain as a result of stroke was reduced and cognitive function was preserved."

Sohrabji and her team plan to continue their work in this area, in hopes of developing a stem cell-derived treatment that could be administered to patients in the aftermath of a stroke to reduce the long-term risk for dementia and other adverse effects.

Story Source:

Materials provided by Texas A&M University. Original written by Luke Henkhaus. Note: Content may be edited for style and length.

---

Journal Reference:

1. Yumna El-Hakim, Kathiresh Kumar Mani, Kaylin A. Pickle, Zara Akbari, Nadia Samiya, Chloe Pham, Gianna Salas, Rachel Pilla, Farida Sohrabji. Peripheral, but not central, IGF-1 treatment attenuates stroke-induced cognitive impairment in middle-aged female Sprague Dawley rats: The gut as a therapeutic target. Brain, Behavior, and Immunity, 2024; 122: 150 DOI: 10.1016/j.bbi.2024.08.008

Gut Bacteria Could Hold the Key to Promoting Healthy Aging

 Your competent? doctor needs to figure out how to get this gut bacteria. Oh, you don't have a functioning stroke doctor willing to do this necessary work, do you?

Gut Bacteria Could Hold the Key to Promoting Healthy Aging

Summary: Certain gut bacteria may play crucial roles in aging, with implications for promoting healthier aging. Research conducted on over 200 octogenarians found a decline in key bacteria, such as Faecalibacterium prausnitzii, and a compensatory increase in other species that help maintain gut health.

These changes impact inflammation, blood sugar, and vitamin levels, suggesting gut bacteria as potential markers for aging. Researchers are now investigating whether these bacterial shifts could be harnessed for therapeutic formulations aimed at enhancing health in aging populations.

Key Facts:

• Gut diversity decreases with age, impacting critical functions for gut health.
• Loss of Faecalibacterium prausnitzii prompts an increase in other butyrate-producing bacteria, supporting gut health.
• Some bacteria correlate with key health markers, like blood sugar and vitamin levels, making them potential indicators of healthy aging.

Source: ASTAR

A new study has revealed that gut bacteria may play a key role in aging, and that specific microbes could be targeted to promote healthy aging.

The Nature Communications study was conducted by scientists from the Agency for Science, Technology and Research Genome Institute of Singapore (A*STAR GIS), in collaboration with researchers from the A*STAR Singapore Immunology Network (A*STAR SIgN), A*STAR Institute for Human Development and Potential (A*STAR IHDP) and the National University of Singapore (NUS).

Aging is a complex, multi-factorial phenomenon with progressive decline in several physiological functions. As Singapore faces a rapidly growing aging population, researchers are seeking ways to understand the aging process and identify key lifestyle and dietary factors to encourage healthy aging.As part of this effort, the team conducted the first large-scale study on over 200 octogenarians (people aged 80 – 89) in Singapore.

Their investigation revealed how the gut microbiome changes with age, highlighting key microbial species associated with aging, and their potential effects on health.

Using advanced DNA sequencing, the research team discovered a significant decrease in gut bacterial diversity as individuals age.

A particularly noteworthy finding was the decline of Faecalibacterium prausnitzii, a crucial bacterium responsible for producing butyrate—an essential short-chain fatty acid that maintains gut health, reduces inflammation, supports gut barrier function, and facilitates gut-brain communication.

Researchers observed an increase in Alistipes and Bacteroides species, with Alistipes utilising alternative substrates from Bacteroides to generate butyrate.

This notable switch may compensate for the reduction of F. prausnitzii, enhancing the metabolic capacity of the elderly gut to produce butyrate and promoting healthier aging.

The team then turned to preclinical models of healthy aging to validate their findings from the human cohort.

Despite differences in the microbes present in different host species, the researchers made a surprising discovery that they had remarkably similar functional enrichments, particularly in pathways related to butyrate production.

This indicates that although the specific microbes may differ across species, the functional roles they play in fostering healthy aging may be similar.

Additionally, the research team examined the association between gut bacterial changes and health markers such as inflammation, blood sugar and vitamin levels.

They identified Parabacteroides goldsteinii, a promising probiotic species associated with fasting blood glucose levels, as well as key gut species like Streptococcus parasanguinis and Bacteroides coprocola, which were linked to serum Vitamin B₁₂ levels, suggesting that these bacteria may serve as indicators for monitoring healthy aging.

Recognising the potential of these associations, the researchers envisaged the development of non-invasive tests for frailty based on gut bacteria analysis.

In the next phase of their research, the team plans to further investigate the identified microbial strains and their metabolic pathways. By using preclinical testing, they aim to explore how these findings can be potentially translated into formulations that promote healthy aging.

Aarthi Ravikrishnan, the lead scientist of the study from A*STAR GIS, commented, “Our research offers key insights into the unique aspects of the gut microbiome and the metabolic shifts associated with aging.

“This study opens exciting new avenues for exploring the biology of aging, with a particular focus on populations in Asia.”

Associate Professor Niranjan Nagarajan, Associate Director, Genome Architecture, and Senior Group Leader, Laboratory of Metagenomic Technologies and Microbial Systems at A*STAR GIS, added, “Our findings lay the groundwork for future research aimed at developing targeted probiotic and prebiotic therapies to enable healthy aging through gut microbiome modulation.”

Dr Wan Yue, Executive Director at A*STAR GIS, commented, “This study has unveiled a better understanding and characterization of the gut microbiome in our local aging population and the potential biomarkers or probiotics unique to the Asian population that can improve healthy aging and to identify individuals at risk for aging-associated diseases.

“This can serve as a useful marker for early detection of diseases and interventions, improving patient prognosis.”

About this microbiome and aging research news

Author: Shu Chian Tay
Source: ASTAR
Contact: Shu Chian Tay – ASTAR
Image: The image is credited to Neuroscience News

Gut Bacteria Linked to Alzheimer’s Progression

 Will your competent? doctor guarantee that this bacteria won't get to you while in the hospital? You better ask now so preventions will exist before you need them.

Gut Bacteria Linked to Alzheimer’s Progression

Summary: Researchers have discovered that the gut bacteria Klebsiella pneumoniae can migrate to the brain, leading to inflammation and cognitive decline that mimic Alzheimer’s symptoms. The study suggests that hospital-acquired infections combined with disrupted gut microbiomes may increase the risk of developing neurodegenerative diseases.

Using a mouse model, scientists found that antibiotic exposure can cause microbiome imbalances, allowing K. pneumoniae to reach the brain. This study opens new avenues for preventing Alzheimer’s by managing infections and gut health.

Key Facts:

• Klebsiella pneumoniae can migrate from the gut to the brain, triggering neuroinflammation.
• Disrupted gut microbiomes after antibiotic use may contribute to Alzheimer’s risk.
• The study emphasizes the role of hospital-acquired infections in neurodegenerative diseases.

Source: FSU

A groundbreaking study by researchers at Florida State University’s Gut Biome Lab has revealed a potential link between an infection caused by gut bacteria and the progression of Alzheimer’s disease.

The research found that the bacteria Klebsiella pneumoniae — a common bacteria notorious for causing hospital-acquired infections — can migrate from the gut into the bloodstream and eventually into the brain.

This bacterial invasion may lead to increased inflammation in the brain and impair cognitive functions, mimicking symptoms seen in Alzheimer’s patients.

The findings emphasize the potential risk hospital-acquired infections like K. pneumoniae may pose in the development of neurodegenerative diseases. Credit: Neuroscience News

The work was published in The Journal of Infectious Diseases.

“Hospitalizations and ICU stays, combined with antibiotic exposure, may lead to a further decline in microbiome diversity that leaves older adults at high risk not only for digestive issues but also for extra-intestinal pathologies such as neurodegenerative disorders through a dysregulation of the gut-brain axis,” said Ravinder Nagpal, an assistant professor in the FSU College of Education, Health, and Human Sciences and the director of the Gut Biome Lab.

The study is the first to show a direct correlation between K. pneumoniae infection and Alzheimer’s pathology, fueling the emerging field that investigates how infectious agents may trigger or aggravate Alzheimer’s disease.

It also paves the way for future research into how to treat harmful infectious agents in vulnerable populations such as the elderly or those recovering from sepsis.

The research suggests that when antibiotics disrupt the gut, it can lead to issues not just in the gut but also in the brain. Using a preclinical mouse model, researchers showed that antibiotic exposure depletes gut bacterial diversity and causes microbiome imbalance, which promotes the proliferation of K. pneumoniae by creating a favorable niche.

When this happens, K. pneumoniae can move from the gut into the bloodstream by passing through the gut lining and eventually reach the brain, triggering neuroinflammation and neurocognitive impairment. 

The findings emphasize the potential risk hospital-acquired infections like K. pneumoniae may pose in the development of neurodegenerative diseases.

“Hospital-acquired and septic infections are one of the risk factors that may increase the predispositions to future neuroinflammatory and neurocognitive impairments, especially in older adults,” Nagpal said.

The study highlights the need for innovative therapeutic approaches to combat the rising prevalence of Alzheimer’s disease, in addition to existing amyloid and tau protein therapies. Further research could provide insight into preventive strategies aimed at managing hospital-acquired pathogens and preserving cognitive health in aging populations.

Funding: The research was funded by the Infectious Diseases Society of America and the Florida Department of Health.

The paper was co-authored by graduate researchers Ian Park, Saurabh Kadyan, and Nathaniel Hochuli from the FSU College of Education, Health, and Human Sciences. Additional collaborators included Hazel K. Stiebeling Professor Gloria Salazar; Associate Professor of psychology and neuroscience Aaron Wilber; University of Florida researchers Orlando Laitano, Paramita Chakrabarty, and Philip A. Efron; and Wake Forest University School of Medicine Associate Professor M. Ammar Zafar.

About this Alzheimer’s disease and microbiome research news

Author: Bill Wellock
Source: FSU
Contact: Bill Wellock – FSU
Image: The image is credited to Neuroscience News

Original Research: Open access.“An Enteric Bacterial Infection Triggers Neuroinflammation and Neurobehavioral Impairment in 3xTg-AD Transgenic Mice” by Ravinder Nagpal et al. Journal of Infectious Diseases

First Gut Microbiome Map for Personalized Food Responses

 How will your competent? doctor use this to optimize your gut-brain axis to get to stroke recovery? 8 years to become competent? DID YOUR DOCTOR SUCCEED?

Do you prefer your  doctor, therapist and hospital  incompetence NOT KNOWING? OR NOT DOING?

gut-brain axis (23 posts to June 2016)

First Gut Microbiome Map for Personalized Food Responses

Summary: A recent study has mapped how molecules in food interact with gut bacteria, revealing why people respond differently to the same diets. By examining 150 dietary compounds, researchers found that these molecules can reshape gut microbiomes in some individuals, while having little effect in others.

This breakthrough could enable personalized nutrition strategies to better manage health risks. The findings offer a deeper understanding of the gut microbiome’s role in health and disease.

Key Facts:

• Gut bacteria respond differently to the same food molecules in different people.
• The study mapped 150 food compounds’ effects on gut microbiomes.
• This research could lead to personalized dietary recommendations for better health.

Source: Yale

“Gut health” is a growing buzzword for foodies and dietitians alike—and with good reason. The trillions of microbes and bacteria living in our gut are implicated in numerous aspects of health and disease.

Scholars at the Yale Microbial Sciences Institute have taken an important step toward evidence-driven personalized nutrition tailored to individual gut health needs.

The lab of Andrew Goodman has generated the first systematic map to show how the molecules in certain foods interact with our unique gut bacteria.

Predicting how an individual responds to a given food—and ultimately how this affects their health—remains difficult. Credit: Neuroscience News

Their findings are published in the journal Cell.

Building on earlier research examining medical drugs and gut bacteria, the scientists set out to understand why different people respond differently to the same foods.

“We know that diet is a huge component of our health and shapes our microbiome,” explained Elizabeth Culp, a former postdoctoral fellow in the Goodman Lab and first author of the study.

While a large body of work has described the effects of “macronutrients” such as fiber on our gut microbiomes, surprisingly little is known about how other small molecule components in food drive health issues.

“Aside from anecdotal examples in the scientific literature, evidence is scarce regarding which dietary changes people can make to help them manage risk factors for diseases like diabetes or cancer,” said Culp.

“It is possible this is because our microbiomes respond differently to the same molecules present in food.”

The scholars designed a systematic map of the interactions between small molecules in our food and different bacteria in the gut.

The work is among the first to describe the specific microbial genes responsible for metabolic transformation of dietary compounds and the mechanisms for how dietary compounds change our microbiomes.

Using liquid chromatography-mass spectrometry at the Yale West Campus Analytical Core, the scientists combined different molecules with gut bacteria to create growth models and maps for around 150 dietary “xenobiotic” compounds.

Sequencing at the Yale Center for Genome Analysis enabled the team to measure the degree of change in the composition of human gut communities.

“We were surprised by the level of variability,” said Goodman, who is the C.N.H. Long Professor and Chair of Microbial Pathogenesis, and Director of the Microbial Sciences Institute (MSI).

“The same dietary compound could dramatically reshape some individuals’ gut microbial communities while having almost no impact on other people’s microbiomes,”

The molecular map provides a mechanism to explain these variable responses between different people, showing how a dietary compound impacts the growth of gut microbes and how that compound is metabolically altered by the microbial community.

Predicting how an individual responds to a given food—and ultimately how this affects their health—remains difficult. But the findings offer a foundation to understand how metabolic reactions vary between people and how these differences shape the growth of “good” or “bad” bacteria in our gut.

“If we can figure out the specific microbial genes that determine how a microbiome responds to a molecule in our food, and how these genes are different between different people’s microbiomes, correlations to diseases like cancer, diabetes, or gastrointestinal infections can start to make sense,” concludes Culp, who is currently a scientist at Empress Therapeutics in Boston.

“This is the first step towards creating custom dietary recommendations as part of personalized nutrition strategies.”

About this microbiome and diet research news

Author: Jon Atherton
Source: Yale
Contact: Jon Atherton – Yale
Image: The image is credited to Neuroscience News

Original Research: Open access.
“Microbial transformation of dietary xenobiotics shapes gut microbiome composition” by Elizabeth J. Culp et al. Cell