Microbiome & Chronic Diseases

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Disease ⇒ Amyotrophic lateral sclerosis {40000171}

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Amyotrophic lateral sclerosis
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References Notes

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Shared Reference Notes

  • [1.8
    - Nicotinamide produced by the Akkermansia muciniphila bacteria slowed disease progression and prolonged survival in an ALS mouse model.
    - Nicotinamide benefits may be linked with improvements in mitochondria function.
    - Nicotinamide and its intermediary molecules significantly reduced in ALS.
    - Nicotinamide levels were decreased in the brains of ALS patients; this reduction was associated with enhanced muscle weakness.
    - Ruminococcus torques and Parabacteroides distasonis worsened ALS symptoms (1)
  • [1.9
    - IL-8, IL-15, MCP-1 and VEGF-A levels were significantly lower in patients than controls, while others did not show a different distribution among groups.
    - IP-10 levels were positively correlated with survival.
  • - The fecal SCFA concentrations (µmol/g) were not significantly different between ALS patients and controls, or between patients with different clinical characteristics.
  • [1.6
    - Greater abundance of Ruminococcus, at genus level > related to higher risk of ALS.
    - Kynurenine > risk factor of ALS.
  • [1.11
    - In spinal motor neurons human induced pluripotent stem cell lines > elevated levels of arachidonic acid.
    - Pharmacological reduction of arachidonic acid levels > reverse ALS-related phenotypes in both human sMNs and in vivo in Drosophila and SOD1G93A mouse models.
  • [1.12
    - ALS in mice> altered bacterial community related to autoimmunity (e.g., Clostridium sp. ASF502, Lachnospiraceae bacterium A4), inflammation (e.g., Enterohabdus Muris,), and metabolism (e.g., Desulfovibrio fairfieldensis) at 1- and 2-month-old SOD1G93A mice, suggesting the early microbial contribution to the pathological changes.
  • [1.7
    - The gut microbial communities of the ALS patients were more diverse and were deficient in Prevotella spp. compared with those of their spouses.
    - Predictive analysis of microbial enzymes revealed that ALS patients had decreased activity in several metabolic pathways, including carbon metabolism, butyrate metabolism, and systems involving histidine kinase and response regulators.

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