Quote: The researchers also found the bacteria was able to prevent the formation of toxic alpha-synuclein clumps by producing chemicals that change how enzymes in cells process specific fats called sphingolipids.
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Quote from your link: The researchers showed that Bacillus subtilis PXN21, a probiotic strain of live bacteria that's available for human consumption, inhibits α-syn aggregation and removes aggregates in C. elegans model with expression of human α-syn. B. subtilis spores induce dietary restriction, which in turn activates the autophagy-lysosomal pathway, a main system of α-syn clearance in cells. This at least partially explains the mechanism of action.
"We therefore asked whether the observed effect on a-syn aggregation is unique to PXN21 or if it is shared among other strains of the B. subtilis species. We tested a panel of laboratory B. subtilis strains, including 168 (Zeigler et al., 2008), JH642 (Smith et al., 2014), and the undomesticated strain NCIB 3610 (Branda et al., 2001). All strains showed similar effects on a-syn aggregation to the probiotic strain PXN21 following the continuous or food-switching regime (Figures 2F and 2G), indicating that the anti-aggregation effect is a general property of the B. subtilis species. Furthermore, all tested B. subtilis strains extended the lifespan of a-syn-expressing transgenic animals (Figure 2H; Table S1)."
My concern is that human trials rarely consider evaluating PD subcategories even though we can only do so crudely if objective. Trials could consider tremor versus no tremor, age PD diagnosed, chemical exposure (e.g. agent orange), other illnesses such as low thyroid, diabetes, high blood pressure which may be related to a cause of PD, and genetic markers if available. A trial may miss that something is successful for a particular group that is a minor part of the whole.
Quotes: Worms raised on a specific strain of B. subtilis, called PXN21, showed a near-total absence of these clumps, compared with worms on other diets. B. subtilis also managed to clear away clumps that had already formed in older worms, which were later switched to the B. subtilis diet. The probiotic’s protective effects lasted over the worms’ lifespan and improved locomotion defects associated with the toxic clumps.
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While encouraging, these findings are quite early and must be corroborated in other settings. Mice, a model organism much more closely related to humans than worms, will be a logical next step. If all goes well and a probiotic-based Parkinson’s therapy makes it to clinical trials, these could be fast-tracked, as probiotic B. subtilis is already commercially available.
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