nature.com/articles/s41522-...
Did I understand this report? No. It is open access, so you get to read it all. There's lots of interesting stuff in the "Discussion" section. I just read through it and hoped something useful would get stuck in my head. I think a few things did:
park_bear should appreciate this: In the present study, the alpha diversity significantly elevated in A53T transgenic monkeys compared to control monkeys (Shannon Index: p < 0.05). Similarly, the alpha diversity also significantly increased in PD patients compared to healthy people25,26. However, the alpha diversity significantly reduced in the rotenone-induced PD mouse model27. Therefore, the rodent model of PD induced by chemical drugs is obviously inconsistent with PD patients and A53T monkeys in the diversity of gut microbiota.
Proteobacteria, Actinobacteria, Eggerthellaceae, and Sphingomonas have been observed to be significantly elevated in PD patients26,28,29. This trend is also observed in the A53T transgenic monkeys with early PD symptoms.
studies have also showed that Lactobacillus, Akkermansia, and Bifidobacteria enrichment are the most commonly identified taxa increased in human PD patients. In our study, Akkermansia was significantly increased in A53T monkeys compared to control monkeys (p = 0.03), which is consistent with the report showed that Akkermansia was significantly related to the greater presence of nonmotor symptoms31.
Barichella et al. have found that Lactobacillus was significant positive associated with human PD patients with severe motor symptoms32, and Unger et al. found that Bifidobacteria were significantly more abundant in PD patients33.
We also observed that Eggerthella lenta significantly elevated in A53T transgenic monkeys, and Eggerthella lenta is a dopamine dehydroxylating strain that can convert dopamine to m-tyramine. M-tyramine is a chemical for regulates neurotransmitters, which was significantly elevated in the urine of patients with neurosis34.
we summarized a comprehensive comparison of intestinal microbiota among Parkinson’s patients, A53T transgenic monkeys, and A53T transgenic mice, and in general, the monkeys at early PD showed consistent gut microbiota with human PD patients.
Metabolites are the ultimate embodiment of cellular activity. Gene expression, splicing, and neuronal function in the brain can be regulated by small-molecule metabolites.
A few previous studies have indicated that changes in short-chain fatty acids are associated with the onset of PD33,35.
Our results also indicate that short-chain fatty acids (butyric acid, isovaleric acid, propionic acid, valeric acid, and isobutyric acid) in the A53T transgenic monkeys showed the trend of reduction compared to control monkeys.
A study has proven that the glyceric acid in the colonic contents of autistic mice also significantly elevated after transplantation of stool from autistic patients36.
Myristic acid and 3-Methylindole were significantly decreased in the A53T monkeys compared with the control monkeys. Myristic acid is an enhancer of diacylglycerol kinase (DGK) δ expression in mouse. DGK is a lipid-metabolizing enzyme that phosphorylates diacylglycerol to produce phosphatidic acid. Decrease in Myristic acid production results in the deficiency of DGKδ, and subsequently induces obsessive-compulsive disorder (OCD)-like behavior through enhancing axon/neurite outgrowth in DGKδ-KO mice43,44,45. Myristic acid and 3-Methylindole were associated with ABC transporters, ABC transporters are the largest class of transporters widely found in bacteria and humans, which can hydrolyze ATP and provide energy to cells.
Parkinson’s and vagal nerve stimulation, promising human studies.
