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Re: Amatuer17 post# 224591

Sunday, 12/15/2019 9:49:50 PM

Sunday, December 15, 2019 9:49:50 PM

Post# of 461142
Xena is correct and therefore Anavex is investigating this as part of its ongoing clinical trials. See these references:

“...the microbiota is closely related to neurological dysfunction and plays a significant role in neuroinflammation through the secretion of pro-inflammatory cytokines. Changes in the homeostatic state of the microbiota leads to increased intestinal permeability, which may promote the translocation of bacteria and endotoxins across the epithelial barrier, inducing an immunological response associated with the production of pro-inflammatory cytokines. The activation of both enteric neurons and glia cells may result in various neurological disorders.”

Gut Microbiota and Their Neuroinflammatory Implications in Alzheimer’s Disease
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6266223/pdf/
nutrients-10-01765.pdf

For example, "In a susceptible individual, inflammatory triggers (1) initiate immune responses in the gut that deleteriously impact the microbiota, increase intestinal permeability, and induce increased expression and aggregation of aSYN (2). Synucleinopathy may be transmitted from the gut to the brain via the vagus nerve (3b), and chronic intestinal inflammation and permeability promote systemic inflammation, which, among other things, can increase blood-brain barrier permeability (3a). Intestinal inflammation, systemic inflammation, and synuclein pathology in the brain all promote neuroinflammation (4) which drives the neurodegeneration that characterizes PD."

The gut-brain axis: is intestinal inflammation a silent driver of Parkinson’s disease pathogenesis?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5445611/

https://www.anavex.com/anavex-life-sciences-presents-new-clinical-data-identifying-gut-microbiota-biomarkers-associated-with-improved-clinical-response-in-patients-treated-with-anavex2-73-at-2019-alzheimers-a/

"Communication between gut microbiota and the brain has been shown to be a critical requirement of a healthy brain function. The reduction in gut microbiota diversity has become one of the hallmarks of aging, and disturbances in its composition are associated with several age-related neurological conditions, including Alzheimer’s disease. These changes in the gut microbiota composition induce increased permeability of the gut barrier and immune activation leading to systemic inflammation, which in turn may impair the blood-brain barrier and promote neuroinflammation, neural injury, and ultimately neurodegeneration.[4]" Giau, V.V.; Wu, S.Y.; Jamerlan, A.; An, S.S.A.; Kim, S.; Hulme, J. Gut Microbiota and Their Neuroinflammatory Implications in Alzheimer’s Disease. Nutrients 2018, 10,
1765

https://www.anavex.com/anavex-life-sciences-presents-new-clinical-data-identifying-gut-microbiota-biomarkers-associated-with-improved-clinical-response-in-patients-treated-with-anavex2-73-at-2019-alzheimers-a/

"The data, presented at the Alzheimer’s Association International Conference, represent the first microbiome measurements reported in a clinical trial of an investigational Alzheimer’s therapy. Because they come from a single sample taken from a small group in an extension study, without a baseline comparator, it’s impossible to know what these associations mean. But the findings are enough to nudge Anavex Life Sciences into adding microbiome changes to its new study of Anavex 2-73, according to Christopher Missling, PhD, president and chief executive officer of the company."

"Things shifted dramatically in 2017, with a seminal paper finding that germ-free mice inoculated with stool from Parkinson’s patients developed Parkinson’s symptoms. This study was widely heralded as a breakthrough in the field—the first time any neurodegenerative disease had been conclusively linked to dysregulations in the human microbiome."

Dr. Missling said ..... "It’s something of great interest, we think, and deserves to be investigated."

https://www.neurologyreviews-digital.com/neurologyreviews/nr_november_2019/MobilePagedArticle.action?articleId=1535393#articleId1535393
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