Strong gut/microbiome link to Parkinson's - possilbe relevance to ME/CFS

[Simon]

@Simon (or anyone),any opinion on how representative is their "mouse model"?

Good question. Using alpha synuclein, the key molecule in PD looks like a strong start. Some comment in a Medcape piece Gut Microbiome Again Linked to Parkinson's Symptoms

Another caveat is that the α-synuclein--expressing mouse model only recapitulates the earlier symptoms of Parkinson's disease, and models for later stages of the disease have not yet been developed, Dr Sampson (lead author] said.

James Beck, PhD, vice president of scientific affairs for the Parkinson's Disease Foundation, echoed the concern that mouse models in Parkinson's disease research have in the past failed to deliver in human trials but said the new findings are nevertheless promising.
"It's important to first note that this is a mouse study because too often we have seen success in treating Parkinson's disease in mice, and the effects haven't translated to humans," he told Medscape Medical News.

"But with that in mind, I think this is really exciting because it opens up a new area of research."

This is not really 'new' new. This came out over a year ago:
Parkinson's disease begins in the gastrointestinal tract, large study indicates

That's quite different, looking at the effect of cutting the vagal nerve on PD risk - nothing about the microbiome.
Vagotomy and subsequent risk of Parkinson's disease - Svensson - 2015 - Annals of Neurology - Wiley Online Library
However, the study itself is questionable because people had their vagal nerve cut because of serious gut issues especially ulcers - so there are all sorts of confounding factors likely too be at play. Comparing them with 'matched' healthy controls, who presumably never had ulcers, isn't necessarily that informative - though a halving of risk for PD is an impressive effect.

Also, the same study is cited as 'controversial' evidence that PD spreads by activation of alpha-synuclein from the gut up the vagal nerve to the brain (as opposed to viruses). Somethiiing for everyone.

 

[Marco]

@Marco too. If I understand you right, you're saying that the mouse model is simply susceptible to inflammation, and any source will do?

A couple of observations on that:
1. There are already plenty of studies linking the gut and microbiome to PD, so they didn't just do a study and say "ha, that's the answer' and I think that needs to be factored in to any interpretation
2.
Smoking strongly reduces the risk of PD, suggesting that generic inflammation doesn't trigger PD.

As I see it, they show that in a synuclein enriched brain, activated microglia leads to clumping. SCFAs can activate microglia but so can many other things including psychological stress - they're pretty promiscuous that way.

Always good for us smokers to see one of the rare upsides . Why that may be the case is an interesting question.

 

[Barry53]

Sarah Myhill discusses leaky gut at drmyhill.co.uk/wiki/Leaky_gut_syndrome_-_a_problem_when_things_go_wrong ...

and gut fermentation ME/CFS at drmyhill.co.uk/wiki/Fermentation_in_the_gut_and_CFS.

 

[roller]

As I see it, they show that in a synuclein enriched brain, activated microglia leads to clumping. SCFAs can activate microglia but so can many other things including psychological stress - they're pretty promiscuous that way.

Always good for us smokers to see one of the rare upsides . Why that may be the case is an interesting question.

These results show that nicotine and hydroquinone inhibit α-synuclein fibrillation and stabilize soluble oligomeric forms. This information can be used to understand the molecular mechanism of the nicotine and hydroquinone action to develop therapeutic solutions for PD.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2647853/

 

[roller]

i think there may be a connection between rabies and PD.

e.g. missing rabies-VNA (virus neutralizing antibodies) in the cfs of PD patients.

how many of PD patients had a rabies vaccination, previously.

 

[Jo Best]

Re. UK - "Dr Fluge is visiting Norwich to collaborate over another Rituximab trial being carried out on the Norwich Research Park. Professor Simon Carding from the Institute of Food Research (IFR) and University of East Anglia will also be talking about at the event about this, as well as research in his own group, who are looking for causes and treatments for ME in the gut and its microbial communities." http://www.ifr.ac.uk/news/events/2017/01/mecfs-biomedical-research/

 

[AndyPR]

@Simon has written a blog about this study for the Microbe Discovery Project, http://microbediscovery.org/2016/12...-is-a-big-step-forward-in-microbiome-science/

New research on Parkinson’s disease, provides the best evidence yet that the gut microbiome can trigger inflammation in the brain, causing disease. Mady Hornig thinks a microbiome-brain link might play an important role in ME/CFS.

The new study, published in the prestigious journal Science, was done on mice. The mice were genetically engineered to develop Parkinson’s disease-like problems of movement and balance, as well as the molecular hallmarks of the disease. However, the researchers found that these mice didn’t develop symptoms if they were reared in a germ-free, sterile environment where they have no gut microbiome. Mice reared in normal, non-sterile conditions developed symptoms, but improved when treated with antibiotics (which kill off gut bacteria), again implicating a role for the microbiome.

 

[Womble]

I know this is an old thread, but:

After having ME/CFS for decades, I developed a complex movement disorder from experimenting with probiotics that influence stomach bacteria.

I also know of ME/CFS patients who actually developed Parkinsons after decades of ME/CFS.

I am convinced there is a strong link here, this needs to be investigated further.