Bile acid modulation by gut microbiota: a bridge to understanding cognitive health

Abstract

The gut microbiota plays an important role in regulating the body's physiological system, and more recently its impact on bile acid metabolism and cognitive function has been investigated by many studies. In addition to their conventional function in fat digestion and absorption, bile acids are now considered crucial signaling molecules that control several metabolic processes and immunological responses. For this purpose, the authors conducted comprehensive research using relevant terms in an attempt to understand more about the gut microbiota and its impact on bile acid metabolism and cognitive health. The gut-brain axis refers to the network of routes through which gut bacteria communicate with the brain. Through its capacity to bio-transform primary bile acids into secondary bile acids, the gut microbiota plays a significant role in bile acid metabolism. Bile acids function as signaling molecules and act on the brain through nuclear and membrane-bound receptors, influencing neurotransmitter production, neuroinflammation, and neuroplasticity to modify this communication. Any dysregulation in this axis can result in cognitive dysfunction. The link between gut microbiota, bile acids, and cognitive health cannot be ignored. It is imperative to explore this link further by conducting large-scale trials to improve the cognitive health of patients with multiple comorbidities, especially those involving the gastrointestinal tract and nervous system.

Keywords: bile acids; brain health; cognitive function; gastroenterology; gut microbiome; neurology.

Figure 1

Summary of bile acid receptors and their functions. FXR, farnesoid X receptor; PXR, pregnane X receptor; S1PR2, sphingosine-1-phosphate receptor 2; TGR5, Takeda G protein receptor 5; VDR, vitamin D receptor.

Figure 2

Role of bile acid signaling in neurophysiological and neurodegenerative conditions. FXR, farnesoid X receptor; LRRK2, leucine-rich Repeat Kinase 2; NMDA, N-methyl-D-aspartate; TGR5, Takeda G-protein-coupled receptor 5; TUDCA, tauroursodeoxycholic acid; UDCA, ursodeoxycholic acid.