Gut microbiota dysbiosis and aromatic amino acid metabolism alterations: a multi-omics analysis of cognitive impairment following aneurysmal subarachnoid hemorrhage.

Background: Aneurysmal subarachnoid hemorrhage (aSAH) is frequently followed by persistent cognitive impairment, characterized by a complex and multifactorial pathological mechanism. While the role of the "microbiota-gut-brain axis" in neurocognition has garnered increasing attention, the specific ways in which gut microbiota and their derived metabolites might be associated with the development and progression of post-aSAH cognitive impairment remain largely undefined. Consequently, there remains a lack of systematic multi-omics evidence to elucidate these potential underlying associations. Methods: In this prospective observational study, we enrolled 48 patients with intracranial aneurysms. Among them, patients with aSAH ( Results: Fecal metagenomics revealed distinct gut dysbiosis in aSAH-CI patients, characterized by reduced alpha diversity, depletion of beneficial commensals (e.g., Conclusion: Our findings suggest a potential dual-hit correlative signature via the microbiota-gut-brain axis in cognitive impairment following aSAH. We hypothesize that the depletion of aromatic amino acid-producing microbiota correlates with reduced neurotransmitter precursors, theoretically impairing synaptic repair. Concurrently, observed associations among opportunistic pathogens, trace amines, and systemic inflammatory and oxidative stress markers suggest a synergistic effect potentially linked to further neuronal damage.