The Role of Gut Microbiota in the Neuroprotective Effects of Selenium in Alzheimer’s Disease

 How is your competent? doctor possibly using this to prevent your chances of dementia? Oh, you don't have a competent doctor because s/he doesn't even know about this or even that you are likely to get dementia?

Your chances of getting dementia.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here:

The Role of Gut Microbiota in the Neuroprotective Effects of Selenium in Alzheimer’s Disease

• Anatoly V. Skalny,
• Michael Aschner,
• Abel Santamaria,
• Tommaso Filippini,
• Viktor A. Gritsenko,
• Yousef Tizabi,
• Feng Zhang,
• Xiong Guo,
• Joao B. T. Rocha &
• Alexey A. Tinkov

• Abstract

  The objective of the present review was to provide a timely update on the molecular mechanisms underlying the beneficial role of Se in Alzheimer’s disease pathogenesis, and discuss the potential role of gut microbiota modulation in this neuroprotective effect. The existing data demonstrate that selenoproteins P, M, S, R, as well as glutathione peroxidases and thioredoxin reductases are involved in regulation of Aβ formation and aggregation, tau phosphorylation and neurofibrillary tangles formation, as well as mitigate the neurotoxic effects of Aβ and phospho-tau. Correspondingly, supplementation with various forms of Se in cellular and animal models of AD was shown to reduce Aβ formation, tau phosphorylation, reverse the decline in brain antioxidant levels, inhibit neuronal oxidative stress and proinflammatory cytokine production, improve synaptic plasticity and neurogenesis, altogether resulting in improved cognitive functions. In addition, most recent findings demonstrate that these neuroprotective effects are associated with Se-induced modulation of gut microbiota. In animal models of AD, Se supplementation was shown to improve gut microbiota biodiversity with a trend to increased relative abundance of Lactobacillus, Bifidobacterium, and Desulfivibrio, while reducing that of Lachnospiracea_NK4A136, Rikenella, and Helicobacter. Moreover, the relative abundance of Se-affected taxa was significantly associated with Aβ accumulation, tau phosphorylation, neuronal oxidative stress, and neuroinflammation, indicative of the potential role of gut microbiota to mediate the neuroprotective effects of Se in AD. Hypothetically, modulation of gut microbiota along with Se supplementation may improve the efficiency of the latter in AD, although further detailed laboratory and clinical studies are required.(Ask your competent? doctor EXACTLY WHOM is doing this further research!)
  

  This is a preview of subscription content, log in via an institution to check access.