I'm not at all surprised. Bacteria can produce quite a variety of compounds, the idea that some gut bacteria could produce harmful compounds seems pretty obvious.
>"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.
Any indications which bacteria produces these amyloids?
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.
Do we know what GOOD bacteria are or what diet to follow to get them where we want them? Do those same GOOD bacteria help with other things like heart disease?
I did some reading on 'good bacteria' for bone health and my take away was it can depend person to person.
I wouldn't be surprised if there isn't a one sized fits all here. Probably having a big diverse population is better than shooting yourself with a few strains, as we get older we have less diversity of gut bacteria and interesting the younger have the opposite.
I'm unsure how? we're generally consuming the same foods, if not better quality comparatively to younger people?
Older people do drop foods and change diet in response to other things that change with age, like allergies, dentition, digestion, blood pressure or diabetes. Old people aren't just young people with years you accumulate stuff and change your life in response.
I heavily doubt that's the main reason for this difference, but old people diets are a healthcare trope for a reason.
I doubt there is a concrete answer. Many bacteria produce amyloids as a normal part of their body. Amyloids are just one specific type of protein fold stacking on each other, and it is so, so common.
Same thing with SCFAs, they are normally part of the metabolic cycle of many bacteria. Tracking down one of them is nearly impossible from something as complex as the gut microbiome.
What they don't tell you is that you cannot just ingest prebiotics and expect it to do anything. You need to do fecal transplant to really have an effect.
Or potentially significant diet adjustments. Having tried to fix my microbiome I have found probiotics useless but the use of prebiotic fibres to promote species does work slowly.
To be clear: The human microbiome contains hundreds of strains of bacteria, often in an established ecosystem. An FMT introduces hundreds of microbes, usually shifting the entire microviome around.
Probiotics aren't incapable of changing the microbiome, it's just that usually they contain only several strains, usually sourced from food or animals, and not humans, in relatively small amounts, and aren't guaranteed to make lasting changes to the microbiome. But they can. If they're the best you can get, they can be worth trying.
This was written November 13, 2020. At that time, the majority of the community believed that amyloid plaques caused Alzheimers from a paper in 2006.
Since the paper in 2006 drug companies that spent billions of dollars in a race for a drug to decrease amyloid plaques to slow down or prevent Alzheimer's. In the trials last year, they found that while the drugs did decrease amyloid plaques, they did not impact Alzheimer's symptoms.
If the new theory of beta-amyloid proteins linked to Alzheimer's proves to be true then someone should look into if there's a link between gut and beta-amyloid proteins.
No, the fact that amyloid-beta or at least its precursor protein APP is causative in Alzheimer's disease is based on very solid science, with a huge amount of genetic evidence behind it.
Lecanemab an antibody that binds to amyloid-beta, is disease-modifying and slows down cognitive deterioration.
The paper from 2006 carried no significance for any of this and it had only minor impact on Alzheimer's disease research.
There has been discussion to whether the plaques of amyloid-beta protein are disease-causing or not. I, as probably most others, believe the plaques as such are non-causative, and that the damage from amyloid-beta happens when amyloid-beta is in a soluble state.
My “street smarts” tell me this is correct. Social isolation combined with filling their guts with someone’s industrial science experiment on a bun ..day in and day out for decades, McDonalds in the morning seems like it is often the last daily grind for America’s army of disenfranchised single retired men (before the cemeteries and dementia wards take them). Is it causal or correlation? This study makes me think they’re eating themselves into insanity which probably helps keep them in that routine before wiping them out completely. It’s so fucking evil.
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[ 3.1 ms ] story [ 49.1 ms ] threadAn example with orangutans
https://intertheory.org/postmodern-autism.htm
>"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.
Any indications which bacteria produces these amyloids?
I wouldn't be surprised if there isn't a one sized fits all here. Probably having a big diverse population is better than shooting yourself with a few strains, as we get older we have less diversity of gut bacteria and interesting the younger have the opposite.
I'm unsure how? we're generally consuming the same foods, if not better quality comparatively to younger people?
I heavily doubt that's the main reason for this difference, but old people diets are a healthcare trope for a reason.
Same thing with SCFAs, they are normally part of the metabolic cycle of many bacteria. Tracking down one of them is nearly impossible from something as complex as the gut microbiome.
Probiotics aren't incapable of changing the microbiome, it's just that usually they contain only several strains, usually sourced from food or animals, and not humans, in relatively small amounts, and aren't guaranteed to make lasting changes to the microbiome. But they can. If they're the best you can get, they can be worth trying.
Since the paper in 2006 drug companies that spent billions of dollars in a race for a drug to decrease amyloid plaques to slow down or prevent Alzheimer's. In the trials last year, they found that while the drugs did decrease amyloid plaques, they did not impact Alzheimer's symptoms.
see: Evidence Mounts for Alternate Origins of Alzheimer’s Disease Plaques https://nyulangone.org/news/evidence-mounts-alternate-origin...
This led to the discovery that some of the data in the 2006 study was faked.
see: Faked Beta-Amyloid Data. What Does It Mean? https://www.science.org/content/blog-post/faked-beta-amyloid...
The latest theory is now on beta-amyloid proteins.
see: Decreased proteins, not amyloid plaques, tied to Alzheimer's disease https://www.sciencedaily.com/releases/2022/10/221004151217.h...
If the new theory of beta-amyloid proteins linked to Alzheimer's proves to be true then someone should look into if there's a link between gut and beta-amyloid proteins.
Lecanemab an antibody that binds to amyloid-beta, is disease-modifying and slows down cognitive deterioration.
The paper from 2006 carried no significance for any of this and it had only minor impact on Alzheimer's disease research.
There has been discussion to whether the plaques of amyloid-beta protein are disease-causing or not. I, as probably most others, believe the plaques as such are non-causative, and that the damage from amyloid-beta happens when amyloid-beta is in a soluble state.