Intersections of gastrointestinal dysbiosis of the gut microbiome and aging

Table 1 Summary of key gut microbial taxa shifts and functional implications across geriatric syndromes and longevity states

Condition/state	Microbial taxa alterations	Proposed pathophysiological mechanism/biomarker significance
Extreme longevity/centenarians	Enrichment in facultative anaerobes[3,4]; distinct lipid/amino acid metabolic signatures[5,6]	Enhanced cellular detoxification, anti-oxidative response, and metabolic adaptability[5,6]
Frailty	Overall reduced microbial diversity[16]; loss of SCFA-producing species[11,17]	Intestinal barrier hyperpermeability leading to systemic translocation of inflammatory cytokines (inflammaging)[9,10]
Sarcopenia	Global reduction in microbiota diversity[19]; depletion of Bifidobacterium adolescentis[22]	Reduced nicotinic acid-mediated mitochondrial support[22], lower serum SCFA levels, and elevated IL-1/TNF-α impairing muscle protein synthesis[21]
Alzheimer’s disease and mild cognitive impairment	Decreased Firmicutes and Bifidobacterium; increased Bacteroidetes[27,28]	Barrier breakdown facilitating systemic release of pro-inflammatory bacterial products and neuroinflammation[27]
Parkinson’s disease	Reduced populations of Bacteroidetes and Prevotellaceae[29,30]	Altered microbial metabolite profiles (e.g., reduced SCFAs) correlated with gut dysmotility and neurodegeneration[29]
Social isolation and stress	Enriched Prevotella; decreased Faecalibacterium; decreased Firmicutes/Bacteroidetes ratio[36]	Stressor-induced epithelial barrier disruption (leaky gut) and neuroendocrine axis modulation[24,36]

SCFA: Short-chain fatty acid; IL: Interleukin; TNF-α: Tumor necrosis factor-alpha.