Fecal microbiota transfer between young and aged mice reverses hallmarks of the aging gut, eye, and brain

Summary

This experimental study used fecal microbiota transplantation in mice to investigate whether alterations in gut microbiota drive age-related inflammation and functional decline in multiple tissues. Young, old, and aged mice were exchanged microbiota, with metagenomic and metabolomic analysis tracking compositional and functional changes. Transfer of aged microbiota into young mice accelerated CNS and retinal inflammation alongside increased intestinal permeability; critically, these effects were reversed by transfer of young microbiota, suggesting the aging microbiota directly drives systemic inflammaging.

Regional applicability

This is a mouse model study and findings require translation to human ageing populations. However, the mechanistic evidence linking dysbiotic microbiota to inflammaging and multi-organ dysfunction (gut-brain-eye axis) is potentially relevant to understanding age-related disease development in older adults in the United Kingdom and globally. Future human intervention studies in UK populations would be needed to establish whether microbiota-targeted therapies (e.g. prebiotics, probiotics, dietary interventions) could prevent or reverse age-related decline.

Key measures

Gut microbiota composition (metagenomic sequencing), metabolic pathway profiles (metabolomics), intestinal barrier permeability, retinal inflammation (immunohistology), CNS inflammation (protein assays), cytokine signalling, functional protein levels in eye, behavioural testing outcomes

Outcomes reported

The study measured changes in gut microbiota composition, metabolic pathways, intestinal barrier integrity, retinal inflammation, CNS inflammation, and behavioural markers following fecal microbiota transfer between young and aged mice. Transfer of young donor microbiota reversed age-associated inflammatory changes in the gut-brain and gut-retina axes.

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