Tau {90000362}

Shared Reference Notes

• [1.1] 
  - Brain-derived tau is a new blood-based biomarker that outperforms plasma total-tau and, unlike neurofilament light, shows specificity to #Alzheimer’s disease-type neurodegeneration.
• [1.2] [#Alzheimer’s disease] [#Short Chain Fatty Acid] [#ApoE4 allele] 
  - #Amyloid-beta is a necessary factor in AD pathogenesis, its accumulation in and of itself is insufficient for neurodegeneration and cognitive decline. - pathological tau accumulation is closely linked with neurodegeneration and cognitive decline in AD and primary tauopathies. - apolipoprotein E (ApoE) isoforms, which strongly influence AD risk and regulate tau-mediated neurodegeneration, differentially affect the gut microbiota. - microbially produced short-chain fatty acids (SCFAs) are mediators of the neuroinflammation-neurodegeneration axis. - Supplementation of SCFAs to GF TE4 mice resulted in more reactive glial morphologies and gene expression as well as increased p-tau pathology.
• [1.3] [#Alzheimer’s disease] [#Amyloid-beta] 
  - adding #Cinnamon or cinnamaldehyde to a cell medium can reduce tau aggregation, Amyloid β and increase cell viability. - #Cinnamon might be useful for preventing and reducing cognitive function impairment.
• [1.4] [#Alzheimer’s disease] 
  - the whole #Coffee extract, #Caffeine, and #Genistein have biological properties in preventing aggregation, condensation, and seeding activity of the repeat region of tau. - a set of #Coffee compounds capable of binding to preformed tau fibrils.
• [1.5] [#Alzheimer’s disease] 
  - administrating feces of AD transgenic mice to wild-type mice resulted in AD-associated gut microbiota dysbiosis, Tau phosphorylation, and #Cognitive impairment in the wild-type mice. - The oral and gut microbiota of AD patient partners resembled that of AD patients but differed from healthy controls, indicating the transmission of microbiota. - #Butyric acid-mediated acetylation of GSK3β at lysine 15 regulated its phosphorylation at serine 9, consequently impacting Tau phosphorylation.
• [1.6] [#Alzheimer’s disease] 
  - co-housing wild-type mice with AD transgenic mice or giving them AD transgenic mice feces caused AD-associated gut microbiota dysbiosis, Tau phosphorylation, and #Cognitive impairment. - Gavage with #Lactobacillus and #Bifidobacterium restored these changes.
• [#Alzheimer’s disease] - #Butyric acid-mediated acetylation of GSK3β at lysine 15 regulated its phosphorylation at #Serine, consequently impacting Tau phosphorylation.
• [1.7] [#Amyloid-beta] 
  - #Tauroursodeoxycholic acid (TUDCA) reduces Aβ deposition, inhibits the progression of amyloid pathology and suppresses GSK3β activity, thereby reducing tau hyperphosphorylation and microglial cell activation. - TUDCA can bind to the G protein-coupled bile acid receptor 1/Takeda G protein-coupled receptor 5 (GPBAR1/TGR5) in microglial cells, increasing cAMP levels, inducing an anti-inflammatory phenotype of microglial cells, and attenuating inflammatory response
• [1.8] [#Alzheimer’s disease] 
  - C3AR and p-tau were reduced by #Agmatine, which has been reported to improve cognitive decline in AD rats.
• [#Alzheimer’s disease] - #Phenethylamine reduced the p-tau levels in AD patient iPSC-derived neurons. #Phenethylamine, a trace amine, has been associated with reduced risk of AD.

References Notes