The connection between the gut and the brain is being explored in relation to neurological diseases. In this study, researchers investigated if a specific fungus, Candida albicans, can travel from the gut to the brain in mice. They found that in germ-free mice without bacteria, the fungus could indeed cross the gastrointestinal barrier and reach brain tissue. Interestingly, the fungus was often found near activated microglial cells, which are involved in immune responses in the brain. Additionally, the researchers examined the effect of aging on the gut fungal composition in conventionally raised mice. They discovered that while there were several fungal species with potential to cause harm, their abundance did not significantly differ between young and aged mice. These findings suggest that aging alone does not drive changes in the gut fungal community that could lead to brain infections. Instead, major disruptions to the gut microbiota or intestinal barrier are likely necessary for fungal escape and brain infection. Further research could explore these disruptions and their role in neurological diseases.

Age-associated changes in the structure of the intestinal microbiome and in its interaction with the brain via the gut-brain axis are increasingly being implicated in neurological and neurodegenerative diseases. Intestinal microbial dysbiosis and translocation of microbes and microbial products including fungal species into the brain have been implicated in the development of dementias such as Alzheimer’s disease. Using germ-free mice, we investigated if the fungal gut commensal, Candida albicans, an opportunistic pathogen in humans, can traverse the gastrointestinal barrier and disseminate to brain tissue and whether ageing impacts on the gut mycobiome as a pre-disposing factor in fungal brain infection. C. albicans was detected in different regions of the brain of colonised germ-free mice in both yeast and hyphal cell forms, often in close association with activated (Iba-1+) microglial cells. Using high-throughput ITS1 amplicon sequencing to characterise the faecal gut fungal composition of aged and young SPF mice, we identified several putative gut commensal fungal species with pathobiont potential although their abundance was not significantly different between young and aged mice. Collectively, these results suggest that although some fungal species can travel from the gut to brain where they can induce an inflammatory response, ageing alone is not correlated with significant changes in gut mycobiota composition which could predispose to these events. These results are consistent with a scenario in which significant disruptions to the gut microbiota or intestinal barrier, beyond those which occur with natural ageing, are required to allow fungal escape and brain infection.

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