Gut bacteria regulate insulation of nerve fibres...

[MSUK]

Gut bacteria regulate insulation of nerve fibres in the brain

Research suggests gut bacteria may directly affect brain structure and function, and could offer new ways to treat multiple sclerosis and psychiatric conditions...Read more - http://www.ms-uk.org/MSnews

[CureOrBust]

...nerve fibres in the prefrontal cortex of the germ-free animals having thicker myelin sheaths than those in the normal animals.

If I am reading the article correctly, it is saying they actually found thicker myelin on the mice without any gut bacteria?

This articles to me, contains a lot of speculation at this early stage.

[ElliotB]

The findings do seem odd, yet interesting. In any case, this may clairfy why they are excited about the findings:

"“We’ve unlocked a process that puts the brakes on myelin formation in the prefrontal cortex,” says Cryan, “and to our knowledge this is the first study showing a clear relationship between the microbiome and myelination in the brain.” The new findings could, therefore, eventually lead to novel treatments for multiple sclerosis and other demyelinating diseases, based on prebiotics, probiotics, or even fecal transplants, all of which could potentially be used to adjust the exact composition of microbes in the gut."

[CureOrBust]

I can understand that they are excited that they have discovered a possible link between the gut bacteria and the mouse myelin thickness. I guess I would be more interested if the germ (ie bacteria) free mice had thinner myelin (instead of the other way around). Also, it occurred to me after I did the above post, that my non medical understanding of gut bacteria is that they promote if not enable the extraction of nutrients from food. So, would the mice without gut bacteria not have sub optimal nutrition? and therefore, thinking about it as I type, would that not possibly be an explanation for any reduced health such as thinner myelin? for example, do gut bacteria help in the assimilation of B12? Even though its still upside-down, it appears to me to be another uncontrolled variable (ie unaccounted for / non-mentioned / uncontrolled variable) in their study.

[David1949]

Another mouse study! The thing is we aren't mice. Mouse studies seem to be unreliable at predicting results in humans. So why don't they just examine the gut flora in healthy normal humans and compare it to the gut flora of people with MS or other diseases? That would not involve any risk to humans and should not require FDA or IRB approval. That could be done immediately and not have to wait months or years for approval. If there is a difference then they might want to try treating patients by adjusting their gut flora. That part might or might not require approval. This seems like a more meaningful approach and could produce results faster than going first through mouse tests and then maybe monkeys and then several phases of human trials.

We need answers soon, not 20 years from now.

[ElliotB]

Everything you might want to know about why mice are used for medical research:


http://www.livescience.com/32860-why-do ... -mice.html

[MStranslate]

Hi all,

I have written and posted an easy to understand summary of this research on our website that may help answer a few questions. You can read it via the link below. The main outcomes were this:

- In germ free mice (those without gut bacteria and other microorganisms), genes involved in myelination were found to be expressed at higher levels

- These genes were all involved in networks that were related to myelination or neuronal plasticity

- Mice that were germ free, but then exposed to environmental bacteria didn't show these differences, indicating that it is a very dynamic process

- The changes in gene expression were found to result in thicker myelin sheaths in the prefrontal cortex of the germ free mice

- These differences were only found in this specific region of the brain and only in male mice

http://www.mstranslate.com.au/gut-micro ... rs-myelin/

This is very early work and needs further validation, but it is very interesting. The researchers themselves state that this isn't what they were necessarily looking for, it's just the way the experiments turned out.

The most likely scenario here is that some bacteria are having a negative impact or inhibiting these processes. This may help explain previous studies that have shown Copaxone changes the gut bacteria population - it was hypothesised that this may be part of the way that it functions as a treatment. The important thing now will be trying to work out exactly what bacteria (or other microorganisms) are having this effect and how it is happening. As I say in the summary, this would open the door for the potential for dietary and probiotic approaches to treatment, as well as using the technique of faecal transplantation.

Happy to answer any more questions?