Gut-Brain Axis (GBA) Poster
Life Science PostersThe central nervous system and the gastrointestinal (GI) tract communicate with each other through the gut-brain axis (GBA). The GBA, a bidirectional link between the gut and the brain, is a complex network that includes the central (CNS), autonomic (ANS) and enteric (ENS) nervous systems, as well as the hypothalamic pituitary adrenal (HPA) axis. It utilizes neural, immune, and endocrine mediators to coordinate and monitor actions of the GI tract, as well as link the activities of the GI tract to brain functioning.
It has been shown that the microbiome of the gut is a key regulator of the GBA. Gut microbiota can modulate the GBA through several means including the production of neurotransmitters and neurotrophic factors, modulation of the intestinal barrier, interaction with ENS afferents, and regulation of the mucosal immune system. The gut microbiome can also influence brain development and homeostasis as seen by changes in the integrity of the blood-brain barrier and induction of neuroinflammation.
Research on the GBA has been increasing in recent years as it is thought to underly several neurodevelopmental, psychiatric, and age-related disorders including Parkinson’s disease, Alzheimer’s disease, schizophrenia, anxiety, and autism. As such, microbiome-targeted therapies are being investigated for their potential to help treat these neurological and neurodegenerative disorders.
To highlight several of the effects that the gut microbiome has on GBA and CNS functioning, Bio-Techne, in collaboration with Dr. Timothy Sampson, Ph.D. from the Department of Physiology at Emory University School of Medicine, has created a new Gut-Brain Axis (GBA) poster.
Key highlights of this poster include:
- An overview of the neuro-epithelial interface in the gut.
- The impact of gut-derived signals on neuroinflammation and neurodegenerative diseases.
- The alteration of brain structure in response to gut-derived signals.
- The effect of the gut microbiome on microglia homeostasis and activation.