Dysbiosis of gut microbiota and Alzheimer’s Disease

Abstract

Alzheimer's Disease (AD) is a degenerative,  chronic, progressive disease of CNS. Pathological  changes that develop in the course of the disease lead to  memory loss, alteration of thought, and deterioration of  other brain functions. The disease progresses slowly,  resulting in cell death and brain damage (Jiang 2017;  Knopman 2016).  Increased permeability of the intestinal and blood  brain barrier due to microbial dysbosis plays a role in  the pathogenesis of AD and other neurodegenerative  disorders associated with aging. In addition, intestinal  microbiota bacterial populations secrete amyloids and  lipopolysaccharides in large quantities, which may  contribute to the modulation of signaling pathways and  the production of proinflammatory cytokines associated  with the pathogenesis of AD (Jiang 2017). Amyloid  precursor protein (APP) , which constitutes Aβ plaques  and is normally secreted by intestinal bacteria, is  expressed by the enteric nervous system. However, the  accumulation corrupts the CNS functions. Escherichia  Coli and Salmonella Enterica are some of the many  bacterial strains that express and secrete APP and play a  role in the pathogenesis of AD (Tse 2017).  Production and clearance of Aβ in CNS is a  dynamic change and some bacteria and fungi are  amyloid secretions, which disrupt the dynamic balance  of Aβ protein in CNS and increase the amyloid levels.  This causes Aβ protein accumulation in the brain and a  high risk of AD (Hill 2015).It is very important for  cognitive function in serotonin, 95% of serotonin is  synthesized in intestines and intestinal microorganisms  play an important role in the synthesis of serotonin.  There is evidence that serotonin may reduce the  formation of Aβ plaques and thus reduce AD risk (Hill  2015; Jiang 2017).