Microbiota–gut–brain axis (MGBA)

The **microbiota–gut–brain axis** (MGBA) is a complex bidirectional communication system linking the gut microbiome, gastrointestinal tract, and central nervous system via immune, neuroendocrine, metabolic, and direct neural pathways[3][4][5][7]. The MGBA is not a single molecule or receptor but a dynamic network involving host cells, microbial metabolites (e.g., short-chain fatty acids), neurotransmitters, cytokines, and multiple signaling axes, such as the vagus nerve and hypothalamic–pituitary–adrenal (HPA) axis[3][4][6]. The MGBA plays a key regulatory role in brain structure, neurogenesis, myelination, microglial function, and permeability of the blood–brain barrier, as well as affecting emotional and cognitive processes[3][7][9]. Dysfunction of the MGBA and its components is implicated in the pathogenesis of neurodegenerative diseases (e.g., Alzheimer’s, Parkinson’s), neuropsychiatric conditions, substance use disorders, and various inflammatory and metabolic diseases[1][2][6][9]. As a therapeutic concept, the MGBA has inspired the investigation of interventions such as dietary change, probiotics, prebiotics, and fecal microbiota transplantation to modulate gut microbiota and, consequently, brain function and disease outcomes, but it is not itself a molecular drug target such as a receptor or enzyme[4][5][6][9]. **Critical note:** The term **"microbiome–gut–brain axis"** does **not** refer to a specific molecule, gene, protein, or receptor, but rather to a multi-component physiological network[3][4][5][7]. Therefore, it is not considered a canonical therapeutic target in the molecular sense. It is sometimes treated as a therapeutic concept for intervention at the system level (e.g., by modulating gut microbiota), but is not a distinct druggable target.

Other names

microbiome–gut–brain axisgut–brain axismicrobiota–brain–gut axis

Modulation of gut microbiome composition; Alteration of microbial-derived metabolites (e.g., short-chain fatty acids); Regulation of immune and inflammatory pathways; Modulation of neurotransmitter production; Modulation of the hypothalamic–pituitary–adrenal (HPA) axis