Parkinson may begin in the Gut>Vagus nerve>Brain

[Phill4]

I found this article today, and there are some things that I don't understand in terms of the actual process.

http://neurosciencenews.com/parkinsons-gastrointestinal-tract-neurology-2150/


But it is thought stimulating when you come to think that the gut is our second brain, and many neurological problems begin there, so I am not sure it is a bacteria or virus that causes it, and if it is then the genetic predisposition is in this weakness of the body to fight it off or predisposition to the disease itself or both.

I don't know much about parkinson's disease. Any thoughts insight?

 

[Gaby]

Any thoughts insight?

Lets just hope they will not come out with a robotic mindless solution like severing the vagus nerve in order to prevent gut inflammation from reaching the brain. While it sounds absurd, one only has to think that one of the surgical "remedies" to treat stomach ulcers involves cutting a branch of the vagus nerve to the stomach.

They cannot conceive how lifestyle changes (i.e. anti-inflammatory diet, breathing exercises, detox) can heal both the body and the mind through the vagus nerve. Narrow and closed minded view. Typical.

 

[MusicMan]

My mother had a similar thing done to her when she was suffering pancreatic cancer.
They treated the nerves with alcohol in an experimental effort to kill the nerve and reduce the pain signal being fed to the brain.
I don't know the result of that, but I do know that when she died, she was dosed to the max with morphine.
I had not heard of Hulda Clark back then.

 

[Phill4]

Any thoughts insight?

Lets just hope they will not come out with a robotic mindless solution like severing the vagus nerve in order to prevent gut inflammation from reaching the brain. While it sounds absurd, one only has to think that one of the surgical "remedies" to treat stomach ulcers involves cutting a branch of the vagus nerve to the stomach.

They cannot conceive how lifestyle changes (i.e. anti-inflammatory diet, breathing exercises, detox) can heal both the body and the mind through the vagus nerve. Narrow and closed minded view. Typical.

I was thinking the same thing, they might as well chop off the stomach altogether, im sure they would lead in that direction.
What i find important is the conection between the gut nerve and brain though. But im not sure how
It would be the only factor in there.

 

[Korzik18]

Here is a relatively recent article detailing how Parkinson's disease and the gut are related. Does Parkinson’s have us by the short and curli?
Here are some quotes:

For a some time, issues with the gastrointestinal system has been associated with Parkinson’s. For example, gut-related complaints – such as constipation and irritable bowel syndrome – are believed to be risk factors for developing the condition.
Researchers have recently been exploring the bacteria that inhabit the gastrointestinal system in the hope of identifying species of microbes that could be directly influencing the condition. Exactly how these tiny organisms might be doing that, however, remains a mystery.
Now researchers have focused their attention on a particular type of protein that is being produced by some of those bacteria. It is called curli.

Prof Heiko Braak – a German neuroanatomist- propose that Parkinson’s may actually begin in the gut and then spread to the central nervous system (the brain).
Braak and his colleagues found large deposits of the Parkinson’s-associated protein called alpha synuclein nerves surrounding the gut and the vagus nerve. These deposits were present even at very early stages of the condition, which supported his theory that maybe the disease was starting (or ‘originating’) in the gut.
This ‘gut to brain’ theory was supported by the fact that people with Parkinson’s often complaining of gastrointestinal problems (eg. constipation) and some of these issues have been suggested to predate the onset of other Parkinson’s symptoms.
Alpha synuclein is one of the most common proteins in the brain (making up about 1% of the protein in neurons). The exact function of alpha synuclein is not well understood, but the current data suggests that it plays a role in multiple cellular functions – particularly in neurotransmitter release.

But in Parkinson’s, something changes.
For some reason, in many cases of Parkinson’s alpha synuclein protein starts to cluster and clump together. And this “aggregated” form of alpha synuclein appears to become toxic.
The aggregation of alpha synuclein is believed to lead to the appearance of Lewy bodies. They are one of the classic hallmarks of Parkinson’s that a neuropathologist will look for in a postmortem brain in order to give a definitive diagnosis of PD.
Problems begin when the alpha-synuclein protein does not fold properly and amyloid fibrils (proteins) are formed.
And here the most interesting thing is that the intestine, or rather the bacteria living in it, begins to play a fatal role.
Some of the bacteria in our gut have the ability to form amyloid proteins themselves. The most well studied of these bacterial amyloid proteins is called curli, that is produced by Escherichia coli and Salmonella. Large amounts of curli protein bind together to form amyloid fibers.

Curli proteins are involved in the adhesion of these bacteria to surfaces within the gut, cell-cell contacts, and help to promote cell aggregation (“community behaviour”) ultimately aiding in host colonisation. In this manner, curli fibers are involved in ‘biofilm formation’.
One problem with curli fibers is that they are potent inducers of inflammatory responses in the host.
Also curli protein had regions that were shared by alpha synuclein.

In an experiment on rats, scientists found that Rats exposed to curli-producing E. coli bacteria the intestinal also exhibited elevated alpha synuclein protein aggregation in the brain, as well as increased numbers of microglia (the resident immune cells in the brain) and raised levels of inflammation markers.
These results led the researchers to conclude that amyloid proteins being produced by bacteria in the microbiota may be “involved in the origination and maintenance of neurodegenerative disease”.

What can help?

Сatechins (particularly EGCG) is remarkably good at blocking the production of alpha synuclein aggregates.
Independent research groups have demonstrated that the alpha synuclein aggregation inhibitor – EGCG – can reduce the negative effect of curli in mice. The efficacy of EGCG in humans is yet to be thoroughly tested. (Sourse)

«…GTP (green tea polyphenols) is well tolerated and appears to provide, at least, a mild symptomatic benefit in early untreated PD.” (Source)

 

[mrtn]

issues with the gastrointestinal system has been associated with Parkinson’s

Maybe this could also be due to thiamine deficiency? There is research about high dose thiamine and parkinsons, like this one:
An open-label pilot study with high-dose thiamine in Parkinson's disease

 

[Korzik18]

Yes, I have read reviews from people with PD who took high doses of thiamine (B1) from 100 mg (sublingual form) and even 3 or more grams (oral). Many have had positive changes and a slower progression of the disease.

And here is another theory of the pathogenesis of PD.

Maybe this could also be due to thiamine deficiency? There is research about high dose thiamine and parkinsons, like this one:
An open-label pilot study with high-dose thiamine in Parkinson's disease

This study mentions:

..the dysfunction of the thiamine-dependent processes could be a primary pathogenic pathway leading to the death of dopaminergic and non-dopaminergic neurons in PD.

..increasing intracellular thiamine could reduce the alpha-synuclein concentration and then the alpha-synuclein aggregation (Brandis et al., 2006).

We suppose that the improvement of the energetic metabolism of the survivors neurons in the substantia nigra , due to the high doses of thiamine, could lead to an increase of synthesis and release of the endogenous dopamine, to an increase of activity of the thiamine-dependent enzymes, or to a better utilization of the exogenous levodopa (Jiménez-Jiménez et al., 1999; Lu'o'ng and Nguyên, 2012; Costantini et al. 2015).

.. the long-term treatment with the intramuscular administration of thiamine has led to a significant improvement of motor and non-motor symptoms of the patients with PD; this improvement was stable during time and without side effects.

 

[Korzik18]

Leave a link here to Keyhole excellent article on high doses of Thiamine and more from another thread. Suddenly someone will come in handy.

Thiamine (Vitamin B1) - A common deficiency in disorders of energy metabolism, cardiovascular and nervous system dysfunction

Just stumbled upon the following recent research. The original article in Russian, and here's a quote from the article: Researchers from the A. N. Belozersky Institute of Physical and Chemical Biology, together with colleagues from the Karolinska Institute and the Medical and Genetic Research...

cassiopaea.org