Faecalibacterium prausnitzii in neurological disorders: mechanistic links and therapeutic potential along the microbiota–gut–brain axis
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Human observational studies link lower F. prausnitzii abundance to greater severity in Alzheimer disease, Parkinson disease, stroke and multiple sclerosis, but not consistently in autism. Interventional evidence is mostly from rodents, with no human trials of live F. prausnitzii.
Widespread dysbiosis in neurological disorders highlights the critical role of the microbiota–gut–brain axis (MGBA) and the therapeutic potential of probiotics in modulating the central nervous system (CNS). Faecalibacterium prausnitzii , a key butyrate-producing commensal bacterium in the human gut, has attracted broad attention as a candidate next-generation probiotic (NGP). This review aims to describe and discuss the mechanisms of action of F. prausnitzii and its potential in the prevention and management of neurological disorders. Multiple human observational cohort studies indicate that the relative abundance of F. prausnitzii —or the genus Faecalibacterium —is negatively correlated with disease severity in conditions such as Alzheimer’s disease (AD), Parkinson’s disease (PD), stroke, and multiple sclerosis (MS); however, the directionality of this association remains discordant in neurodevelopmental conditions such as autism spectrum disorder (ASD). To date, interventional evidence is predominantly derived from rodent models, in which oral gavage of specific F. prausnitzii strains or synbiotic formulations has been reported to alleviate cognitive deficits, motor dysfunction, anxiety-like behaviors, and pathological protein deposition. Mechanistically, these neuroprotective effects involve diverse F. prausnitzii -derived neuroactive metabolites—including the microbial anti-inflammatory molecule (MAM), extracellular vesicles (EVs), and phenolic derivatives—as well as indirect pathways mediated by butyrate through histone deacetylase (HDAC) inhibition and intestinal barrier fortification. Given the current lack of clinical intervention trials directly administering live F. prausnitzii in human neurological populations, future research requires rigorously designed, strain-specific randomized controlled trials (RCTs) to establish its clinical safety, colonization efficiency, and therapeutic efficacy.
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