AMITY UNIVERSITY GWALIOR MADHYA PRADESH

PRESENTATION TOPIC ON

GUT MICROBIOTA BRAIN AXIS

SUBMITTED TO
Dr SHVETANK BHATT SUBMITTED BY
NEERAJ SUMAN
B.PHARM 7(SEMESTER)
AIP GWALIOR
 INTRODUCTION
• Gut bacteria cooperate with their animal hosts to regulate the development
and function of the immune, metabolic and nervous systems through
dynamic bidirectional communication along the ‘gut–brain axis’. These
processes may affect human health, as certain animal behaviours appear to
correlate with the composition of gut bacteria, and disruptions in microbial
communities have been implicated in several neurological disorders. Most
insights about host–microbiota interactions come from animal models,
which represent crucial tools for studying the various pathways linking the
gut and the brain. However, there are complexities and manifest limitations
inherent in translating complex human disease to reductionist animal
models. In this Review, we discuss emerging and exciting evidence of
intricate and crucial connections between the gut microbiota and the brain
involving multiple biological systems, and possible contributions by the gut
microbiota to neurological disorders. Continued advances from this frontier
of biomedicine may lead to tangible impacts on human health.
 PURPOSE,METHODS ,FINDING AND
IMPLICATION
• Work on animal models has established the microbiota-gut-brain axis as a real phenomenon; to date, the evidence
for its operation in man has been limited and has been confronted by considerable logistical challenges. Animal and
translational models have incriminated a disturbed gut microbiota in a number of CNS disorders, including
Parkinson’s disease; data from human studies is scanty. While a theoretical basis can be developed for the use of
microbiota-directed therapies in neurodegenerative disorders, support is yet to come from high-quality clinical trials.
• anxiety, attention-deficit hypersensitivity disorder (ADHD), autism, cytokines, depression, gut,
hypothalamic–pituitary–adrenal (HPA) axis, inflammation, immune system, microbiota, nervous system,
neurologic, neurotransmitters, neuroimmune conditions, psychiatric, and stress.
• Various afferent or efferent pathways are involved in the MGB axis. Antibiotics, environmental and
infectious agents, intestinal neurotransmitters/neuromodulators, sensory vagal fibers, cytokines, and
essential metabolites all convey information to the central nervous system about the intestinal state.
Conversely, the hypothalamic–pituitary–adrenal axis, the central nervous system regulatory areas of
satiety, and neuropeptides released from sensory nerve fibers affect the gut microbiota composition
directly or through nutrient availability. Such interactions seem to influence the pathogenesis of a
number of disorders in which inflammation is implicated, such as mood disorder, autism-spectrum
disorders, attention-deficit hypersensitivity disorder
• Recognition of the relationship between the MGB axis and the neuroimmune systems provides a novel
approach for better understanding and management of these disorders. Appropriate preventive
measures early in life or corrective measures such as use of psychobiotics, fecal microbiota
transplantation, and flavonoids are discussed.
 OTHER RESEARCH
• The primary reports were reviewed and classified into animal and human data concerning:
modifications of the monoamine receptors in anxiety and depression, pathophysiology of
endocrine factors in anxiety and depression, patho-physiology of the hypothalamic–pituitary–
adrenal (HPA) axis and the pathophysiology of the HPA dysregulation in anxiety and in depression.
In addition, a proposed model of a neuroendocrine continuum for anxiety and depression, in which
anxiety occurs first during the life course and major depressive episodes occur later, was examined.
• Results: Based on the available literature, increased concentrations of corticotropin-releasing factor
(CRF) in the cerebrospinal fluid has been reported in both anxiety and depression. However, release
of other peptides or hormones of the HPA axis is regulated differently in the two disorders. Anxiety
is characterized by hypocortisolemia, supersuppression after dexamethasone and increased
numbers of glucocorticoid receptors, whereas depression is characterized by hypercortisolemia,
non-suppression after dexamethasone and decreased numbers of gluco-corticoid receptors. A
‘neuroendocrine continuum’ model is proposed to explain these differences. A general
desensitization of CRF receptors at pituitary, limbic (amygdala) and cortical as well as hippocampal
levels could be secondary to the loss of hippocampal inhibition resulting from hippocampal damage
linked to repeated stressing events.
• Conclusion: The proposed hypothesis remains to be tested by examination of either the changes in
receptors and neurotransmission or the mech-anisms underlying the dysregulation of endocrine
factors.