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Saturday, July 27, 2019 2:41:24 PM
I am saying there is no data or information in the Anavex presentation to suggest that is the case.
Research does suggest the gut-brain-axis is bidirectional.
The bidirectional nature of the gut–brain axis is also proposed by Cox and Weiner [21]. We recently proposed that in CNS inflammatory diseases the association with the gut microbiota is bidirectional [24]. In nonobese diabetic mice, the induction of EAE promoted a significant change in the overall structure of the gut microbiota, which was more significant in mice that developed severe disease compared with mice that did not develop or developed a milder form of disease. In this context, the disease promoted changes in the microbiota. Similarly, treatment with antibiotics at early stages of disease (from day 0 to 14) resulted in reduced severity of disease, indicating the bidirectional association between disease and the microbiota [24]. The induction of EAE in mice has remarkable cellular and molecular effects on the intestinal barrier by promoting the induction of a “leaky gut” and accumulation of proinflammatory Th17 and Th1 cells, concomitant with reductions in regulatory T cells in the intestinal mucosa [25]. The effects of MS in intestinal barrier disruption are reviewed by Buscarini et al. [6]. These authors discuss the relatively high frequency of intestinal barrier dysfunction in patients with MS, perhaps inherited genetically. The comorbidities of MS and other diseases associated with the intestine, such as Crohn’s disease and other inflammatory diseases, are nicely covered in this review.
The Microbiome and Neurologic Disease: Past and Future of a 2-Way Interaction
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