Disease ⇒ Amyotrophic lateral sclerosis {40000171}

References Notes

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.