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First stool transplant/microbiome transfer = 12.11.2021 (1x200ml)

Second stool transplant/microbiome transfer on September 19, 2022 to October 10, 2022 (10x20ml)

One can clearly see from the findings that the intestinal microbiome has greatly improved after the two microbiome transfers!

Here is an answer (he saw the last report from 1/19/23) from a Prof. Dr. from the research of 6.2.23:

But what has changed in most microbiome studies andParkinson'sshows is the observation that so-called butyric acid producers are reduced. Butyric acid is the main energy of the intestinal cells and if not enough is produced, then this naturally has consequences for the intestinal wall. And you now knowthat Parkinson's probably originated in the gut.

According to their report, the number of these bacteria is even greatly increased. There is no "too much" for this though, this is misleading. So from a microbiological point of view I would say: Looks good.


It is about the specific strains: Desulfovibrio desulfuricans, Desulfovibrio fairfieldensis, Desulfovibrio piger these one should best not have in the intestine! They are said to be probably the trigger of Parkinson's disease. Desulfovibrio is not present in my stool findings, however I need to clarify if the three subgroups mentioned above are also not present.


Also, it should be beneficial to have as few of the following bacterial strains as possible (this is true in my case - see findings) : Cyanobacteria (bacterial strain), Bifidobacterium dentium (neuroactive microbiota), Citrobacter spp. (LPS-bearing microbiota), Enterococcus spp. (immunomodulation + lactate-forming / saccharolytic microbiota), Verrucomicrobiaceae, Bifidobacteriaceae and Christesenellaceae.


With respect to the family level of bacteria, a recent meta-analysis of fourteen case-control studies showed significantly increased relative abundance of Verrucomicrobiaceae, Bifidobacteriaceae, and Christesenellaceae in the gut microbiota of PD by 95% confidence interval analysis (Shen et al., 2021).


At the genus level, a microbiome-wide association study found that opportunistic pathogens such as Porphyromonas, Prevotella, and Corynebacterium are elevated in PD (Wallen et al., 2020)

A case-control study provided broad evidence of DSV dynamics and found that the relative abundance of bacteria in the Desulfovibrionaceae family was increased in the microbiota of PD patients (Lin et al., 2018). 

DSV exhibit several interesting properties that lend themselves to a potential role in PD pathogenesis and warrant further investigation. 

DSV are sulfate-reducing bacteria (SRB) that are commonly found in the environment and human gut and have the potential to cause infections in humans (Loubinoux et al., 2002; Goldstein et al., 2003). As such, DSVs produce hydrogen sulfide (H2S), a metabolite known to affect cell signaling in neuronal cells at low concentrations and pose serious toxicity at higher concentrations (Carbonero et al., 2012; Panthi et al., 2018; Haouzi et al., 2020). H2It has been observed that S releases mitochondrial cytochrome c into the cytosol, where the cytochrome is able to form α-Syn radicals, thereby initiating α-Syn oligomerization (Guo et al., 2015; Kumar et al., 2016). Furthermore, H2S can disrupt iron metabolism by increasing cytosolic iron levels (Cassanelli and Moulis, 2001; Hälldin and Land, 2008), an event that may induce α-Syn aggregate formation (Joppe et al., 2019). DSV have been found to colonize the mucus gel layer of the colon (Nava et al., 2012; Earley et al., 2015).

Therefore, the α-Syn-expressing enteroendocrine cells located in the intestinal wall in close proximity to the intestinal DSV may be particularly susceptible to the toxic effects of H2S and serve as a nucleus for α-Syn aggregation in the nervous system.

In addition, DSV have the ability to reduce ferric iron to ferrous iron using a periplasmic [FeFe] hydrogenase enzyme that is present in virtually all DSV and confers the ability to form magnetite (Fe 3O4) (Chistyakova et al., 2004; Park et al., 2008; Pereira et al., 2011). It has been reported that uncoated magnetite nanoparticles accelerate α-Syn aggregation and are considered to be involved in PD pathogenesis (Joshi et al., 2015; Murros et al., 2019). Since DSV are present in the human gut microbiota and are capable of producing extracellular magnetite and H2S, both of which induce oligomerization and aggregation of α-Syn, it is reasonable to speculate that there may be a correlation between these bacteria and PD.

Here, we used a targeted PCR-based approach to determine absolute quantitative changes in DSV bacterial levels between PD patients and healthy controls.

There are numerous scientific reports on the Internet about this. The whole subject is very complex.

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