4.7 Article

Relevance of gutmicrobiota in cognition, behaviour and Alzheimer's disease

Journal

PHARMACOLOGICAL RESEARCH
Volume 136, Issue -, Pages 29-34

Publisher

ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.phrs.2018.07.007

Keywords

Gut microbiota; Microbiome; Brain; Cognition; Dementia; Alzheimer's disease

Funding

  1. FAPESP (Fundacao de Amparo a Pesquisa de Sao Paulo) [2013/20695-3, 2009/52825-8, 2016/01302-9]
  2. CNPq (Conselho Nacional de Pesquisa Cientifica) [554535/2005-0]

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Approximately 95% of the symbiotic microbes in human body are located in the gut. This microbioma is involved in important homeostatic processes, not only related to gastrointestinal function but also to several complex modulatory processes, such as glucose and bone metabolism, inflammation and immune response, peripheral (enteric) and central neurotransmission. For that reason, recent studies proposed that abnormalities in gut microbiota may play a role in systemic and central nervous system (CNS) conditions. Therefore, the integrity of gut microbiota be relevant to the pathophysiology and control of important medical diseases like diabetes mellitus, inflammatory and autoimmune diseases, and even neuropsychiatric disorders such as depression, autism spectrum disorder, Parkinson's and Alzheimer disease. Gut microbiota may affect brain function and behaviour through the microbiota-gut-brain axis, in bidirectional interplay with top-down and bottom-up regulations. Through metabolic activity of non- pathogenical microorganisms and secretion of functional by-products that increase the permeability of the intestinal mucosa, the gut microbiota influences both the production and absorption of neurotransmitters (e.g., serotonin and GABA), increasing their bioavailability to the CNS. It has been further shown some components of the gut microbiota predominantly bacteria synthesize and release amyloid peptides and lipopolysaccharides, which in turn activate inflammatory signalling through the release of cytokines, with potential effects on the pathophysiological cascade of Alzheimer disease.

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