Microbiome consisting of fungi, bacteria, algae and viruses found in brains of even healthy people

Hip

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A new study has found a thriving microbiome living in the brains of even healthy people.

The most abundant microbes found living in the brain are fungi, bacteria, and chloroplastida (green algae). The significance of having algae living in the brain is not at this stage known. Other unusual microbes found in the brain are amoebozoa, basal eukaryota, and holozoa/metazoa.

Around 20% of the species detected in gut microbiome were present in the brain microbiome.

Adenovirus type C was the major virus found in human brain; other viruses were not well represented. But low levels of herpes simplex 1 virus, Epstein-Barr virus and cytomegalovirus were found.

The authors say finding that adenovirus is the major virus present in the human brain, both in controls and in Alzheimer's patients, is of interest because adenovirus can cause long-term CNS inflammation in animal models.


In terms of how many microbes there are living in the healthy brain, for every one human brain cell, there are
0.14 bacteria and 0.05 fungi. In some of the heavily infected Alzheimer's brains, there were 1.8 microbes for every brain cell.


A newspaper article on this study:
The brain microbiome: could understanding it help prevent dementia?

The article details how sometimes dementia is due to a brain infection, and can be reversed with antimicrobials:
A recent paper she jointly lead-authored, published in Alzheimer’s and Dementia, compiled a long list of case reports where infectious disease was discovered to be the primary cause of dementia, meaning that, in many cases, the dementia was reversible.

A few of the patients died, but most survived and saw significant improvements in cognitive function, including a man in his 70s who had been diagnosed with Alzheimer’s disease after his swift cognitive decline saw him unable to drive or, eventually, leave the house alone. A sample of his cerebrospinal fluid was taken and revealed a fungal infection caused by Cryptococcus neoformans. Within two years of taking antifungal medication, he was driving again and back at work as a gardener.

A common infection among the dementia cases was what the gardener had: C neoformans, a fungus often found in plants and animals, the spores of which are easily inhaled.
 

southwestforests

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This is interesting! 🤔🙂
Both generally and at a personal level since Granddad and Grandma W both got diagnosed with dementia before they passed away.
And Dad is diagnosed with dementia and at least somewhat successfully treated for it.
 

Wishful

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Algae wouldn't have much luck photosynthesizing in the brain, but maybe they make their way in through the nose, and the immune cells identify them as "Doesn't cause trouble, just ignore it."
 

southwestforests

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If this true
I'm expecting it is true and has been true.
Been playing in Google.

Finding things such as,
Do gut bacteria make a second home in our brains?
Preliminary finding turns heads at neuroscience meeting
9 Nov 2018 By Kelly Servick
https://www.science.org/content/article/do-gut-bacteria-make-second-home-our-brains

SAN DIEGO, CALIFORNIA—We know the menagerie of microbes in the gut has powerful effects on our health. Could some of these same bacteria be making a home in our brains? A poster presented here this week at the annual meeting of the Society for Neuroscience drew attention with high-resolution microscope images 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.

In the initial survey of the electron micrographs, Roberts's team observed that resident bacteria had puzzling preferences. They seemed to inhabit star-shaped cells called astrocytes, which interact with and support neurons. In particular, the microbes clustered in and around the ends of astrocytes that encircle blood vessels at the blood-brain barrier. They also appeared to be more abundant around the long projections of neurons that are sheathed in the fatty substance called myelin. Roberts can't explain those preferences but wonders whether the bacteria are attracted to fat and sugar in these brain cells.

Why haven't more researchers seen bacteria in the brain? One reason could be that few researchers subject postmortem brains to electron microscopy, Roberts says. "Pairing up a neuroanatomist with a brain collection just doesn't happen very often." And neuroscientists may—as she did until recently—disregard or fail to recognize bacteria in their samples.
 

southwestforests

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If this true
Another find & I'm not seeing a date on the page, might be there isn't one, might be the script blocker on my browser is blocking it.

Is there a brain microbiome?
Over the past decade, the development of new sequencing technologies has enabled extensive characterization of microorganisms living in or on the human body (the "human microbiome"). In particular, characterization of microorganisms in the gut has led to a deeper understanding of how the microorganisms we coexist with can influence our physiology, immune system, behavior, and overall health. In contrast to the gut microbiome, it is less clear the degree to which microorganisms actually inhabit our tissues and organs, and whether this might also influence our physiology. This relative ignorance results largely because it is much easier to obtain fecal samples than tissue biopsies, particularly of the central nervous system. However, in the course of our analysis of human brain transcriptome data, we have noted a surprisingly high level of microbial sequences, which appear to differ in different brain regions. We are currently investigating the possibility that the microbial sequences we have identified are not simply due to contamination, but actually reflect resident microbes.

https://www.colorado.edu/lab/neurodegeneration/there-brain-microbiome
 

Wishful

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One reason no one has looked for a brain microbiome is because "Everyone knows that the BBB keeps microbes out." There's a famous quote (Einstein?) along the lines of "It's not what we don't know, it's what we do know that is wrong." I wonder whether ME research is hampered by false knowledge. The (false) knowledge that CFS was psychological certainly hampered research, and is still hampering it, since it's hard to counter old false knowledge.
 

southwestforests

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Another find from the history of the concept of brain microbiome,

Neurosci Insights
. 2021 May 27;16:26331055211018709. doi: 10.1177/26331055211018709

Is There a Brain Microbiome?​

Christopher D Link1,✉

PMCID: PMC8165828 PMID: 34104888

https://pmc.ncbi.nlm.nih.gov/articles/PMC8165828/

Why Even Consider a Brain Microbiome?​


A seminal study published by the Power group11 provided intriguing evidence for the presence of microbes in the human brain. These researchers set out to determine if the brain injury observed in HIV/AIDS was accompanied by microbial infiltration into the brain. Using high-throughput sequencing of total RNA from autopsy-derived cerebral white matter, these investigators found non-human sequences aligning to 173 different bacteria and phage. Critically, these researchers found similar distributions of microbial sequences in both the HIV and control brain samples. α-proteobacteria was the predominant phylum of bacteria identified, and was found in all brain samples tested. These observations were validated by both 16S rRNA gene amplification and in situ staining for peptidoglycan and bacterial 16S rRNA sequences. Importantly, these researchers also demonstrated that bacterial sequences detected in a human brain sample by 16S RNA amplification were present in the brains of immuno-compromised mice (Rag−/−) 7 weeks after transplantation of the human brain tissue into the mice. In contrast, parallel transplantation of heat-treated brain tissue into immuno-compromised mice resulted in no or minimal detection of the targeted 16S RNA sequence, suggesting that the 16S RNA sequences detected in the human brain samples were derived from viable bacteria. While this early study used relatively small sample sizes, it provided the types of validation studies needed to counter the common assumption that the brain is sterile.

NOTE that last bit,
the common assumption that the brain is sterile

"Common Assumption" ... there is a lot of that in human health.

Relevant reference,
while it is specifically about doing medical practice, same principle holds true for anatomical and biological belief.

The New York Times
Why Doctors Still Offer Treatments That May Not Help
Evidence-based medicine has made progress since doctors’ infamous bloodletting of George Washington, but less than you might think.
By Austin Frakt
Aug. 26, 2019

https://www.nytimes.com/2019/08/26/upshot/why-doctors-still-offer-treatments-that-may-not-help.html

There are countless other examples of common treatments and medical advice provided without good evidence: magnesium supplements for leg cramps; oxygen therapy for acute myocardial infarction; IV saline for certain kidney disease patients; the avoidance of peanuts to prevent allergies in children; many knee and spine operations; tight blood sugar control in critically ill patients; clear liquid diets before colonoscopies; bed rest to prevent preterm birth; the prescribing of unnecessary medications, to list just a few. In some of these cases, there is even evidence of harm.

It is not uncommon for newer evidence to contradict what had been standard practice. A study by an Oregon Health & Science University School of Medicine physician, Vinay Prasad, and colleagues examined 363 articles in the New England Journal of Medicine from 2001 to 2010 that addressed an existing medical practice. Forty percent of the articles found the existing practice to be ineffective or harmful.

Some of these reversals are well known. For example, three articles contradicted hormone replacement therapy for postmenopausal women. Another three reported increased risk of heart attacks and strokes from the painkiller Vioxx.

Looked at one way, medical reversals like these reflect a failure; we didn’t gather enough evidence before a practice became commonplace. But in another way, they were at least a partial success: Science eventually caught up with practice. That doesn’t always happen.

“Only a fraction of unproven medical practice is reassessed,” said Dr. Prasad, who is co-author of a book on medical reversals, along with Adam Cifu, a University of Chicago physician.
 

southwestforests

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I wonder whether ME research is hampered by false knowledge. The (false) knowledge that CFS was psychological certainly hampered research, and is still hampering it, since it's hard to counter old false knowledge.
Yes, Yes, and Yes.

From that NYT article I quoted some of,

It’s an uphill battle. Even when we learn something doesn’t make us better, it’s hard to get the system to stop doing it. It takes years or even decades to reverse medical convention. Some practitioners cling to weak evidence of effectiveness even when strong evidence of lack of effectiveness exists.

This is not unique to clinical medicine. It exists in health policy, too. Much of what we do lacks evidence; and even when evidence mounts that a policy is ineffective, our political system often caters to invested stakeholders who benefit from it.

An honest assessment of the state of science behind clinical practice and health policy is humbling. Though many things we do and pay for are effective, there is a lot we don’t know. That’s inevitable. What isn’t inevitable — and where the real problems lie — is assuming, without evidence, that something works.
 

Cipher

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It's interesting in this context that amyloid beta has relatively recently been found to be antimicrobial, acting against bacteria, fungi, and viruses. This in combination with the fact that amyloid beta targeting drugs, such as monoclonal antibodies, haven't had much effect in Alzheimer's disease trials, supports the hypothesis that a brain infection might be the underlying cause:

Can an Infection Hypothesis Explain the Beta Amyloid Hypothesis of Alzheimer’s Disease?

Abstract

Alzheimer’s disease (AD) is the most frequent type of dementia. The pathological hallmarks of the disease are extracellular senile plaques composed of beta-amyloid peptide (Aβ) and intracellular neurofibrillary tangles composed of pTau. These findings led to the “beta-amyloid hypothesis” that proposes that Aβ is the major cause of AD. Clinical trials targeting Aβ in the brain have mostly failed, whether they attempted to decrease Aβ production by BACE inhibitors or by antibodies. These failures suggest a need to find new hypotheses to explain AD pathogenesis and generate new targets for intervention to prevent and treat the disease. Many years ago, the “infection hypothesis” was proposed, but received little attention. However, the recent discovery that Aβ is an antimicrobial peptide (AMP) acting against bacteria, fungi, and viruses gives increased credence to an infection hypothesis in the etiology of AD. We and others have shown that microbial infection increases the synthesis of this AMP. Here, we propose that the production of Aβ as an AMP will be beneficial on first microbial challenge but will become progressively detrimental as the infection becomes chronic and reactivates from time to time. Furthermore, we propose that host measures to remove excess Aβ decrease over time due to microglial senescence and microbial biofilm formation. We propose that this biofilm aggregates with Aβ to form the plaques in the brain of AD patients. In this review, we will develop this connection between Infection – Aβ – AD and discuss future possible treatments based on this paradigm.
 
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