Akkermansia muciniphila administration in transgenic Alzheimer's mice reduced amyloid-beta plaques and improved cognitive function by modulating tryptophan metabolism. The bacterium increased beneficial metabolites including indole-3-acetic acid, tryptophan, and short-chain fatty acids like butyrate and acetate, while decreasing inflammatory markers IL-6, IL-1β, and TNF-α. The protective effects occurred through the AhR/NF-κB/NLRP3 signaling pathway. This mechanistic insight represents a significant advance in understanding how specific gut bacteria influence neurodegeneration. The tryptophan-indole pathway has emerged as a critical link between microbiome health and brain function, with indole-3-acetic acid showing particular promise as a neuroprotective compound. While promising, this remains preclinical work in a mouse model that may not fully recapitulate human Alzheimer's complexity. The findings align with growing evidence that gut microbiome interventions could become viable therapeutic strategies for neurodegenerative diseases, though human trials are essential to validate clinical relevance and optimal dosing protocols.
Akkermansia muciniphila reduces Alzheimer's amyloid plaques via tryptophan pathway
📄 Based on research published in Alzheimer's research & therapy
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