Gastrointestinal Dysfunction in Parkinson’s Disease 2021 Jan

[Bolt_Upright]

There is an incredible amount of information about the PK effect on the gastrointestinal system in this paper. Pictures too!

ncbi.nlm.nih.gov/pmc/articl...

This part about the aggregated α-synuclein being all through the gut made me think of mannitol and if it is stopping α-synuclein aggregating in the brain it is doing that in the gut too. And wondering if the aggregated α-synuclein is traveling from the gut to the brain or is it the aggregated α-synuclein in the brain aggregated in the brain?

"Patients show deposits of pathological, aggregated α-synuclein not only in the brain but throughout almost the entire length of the digestive tract. This gives rise to non-motor symptoms particularly within the gastrointestinal tract and patients experience a wide range of frequent and burdensome symptoms such as dysphagia, bloating, and constipation. Recent evidence suggests that progressive accumulation of gastrointestinal pathology is underway several years before a clinical diagnosis of PD. Notably, constipation has been shown to increase the risk of developing PD and in contrast, truncal vagotomy seems to decrease the risk of PD. Animal models have demonstrated gut-to-brain spreading of pathological α-synuclein and it is currently being intensely studied whether PD begins in the gut of some patients. "

Being diagnosed with REM Sleep Behavior Disorder, it has information I sure did not like reading:

"Ideally, these hypotheses about the etiology of PD should be tested in longitudinal human studies, but as it is inherently difficult to study the silent onset of pathology this has so far not been possible. However, a peculiar sleep disorder characterized by disruption of the normal atonia during REM-sleep together with dream enactment has gained interest. Nearly all people with this sleep disorder, called REM-sleep behavior disorder (RBD), progresses to manifest PD or the highly similar condition dementia with Lewy bodies (DLB) within 15 years [41]. The disorder arises as a consequence of damage to certain nuclei in the pons and is the strongest prodromal marker of PD [42]. Remarkably, patients with RBD display a greater density of gastrointestinal LP than patients without [43]. Likewise, loss of cardiac sympathetic innervation and colonic acetylcholinesterase in RBD cases have been shown to be comparable to that of diagnosed PD patients, although the dopaminergic system in the RBD cases was still intact [44]. Consequently, it has been proposed that RBD represents a prodromal biomarker of a gastrointestinal, body-first onset of PD [45]."

I'm a bit hopeful about this part. I'm the prodromal they are talking about:

"Overall, widespread pathology of the gastrointestinal tract is indeed present already in prodromal stages of PD at least in a considerable fraction of cases."

No real answers, but information to base my uneducated decisions on.

Bolt

[park_bear]

You are intervening much earlier than anyone else so that is very good.

High dose thiamine helped my GI tract.

[Bolt_Upright in reply to park_bear]

Thank you park_bear.

[Hidden]

I am intervening very proactively too. Bolt, I no am grateful for all your information and research. And, your very proactive nature is uplifting to me. I feel less alone in this. The pathology of Lewy Body dementia has a lot of similarities to ALZ. Therefore, I recommend expanding your research to what is helpful to ALZ in addition to PD. ALZ has been studied and invested in far more than LBD.

You should listen to Dr. Dale Bredeson. Some think he’s a quack. I do not. He has studied ALZ for 30 years at the Buck Institute in CA.

[Bolt_Upright in reply to Hidden]

Thanks CC. I have his book and belong to his FB group. I like his point about removing insults to the body. Good luck and may God Bless You.