Does Alzheimer's disease stem in the gastrointestinal system?

The potential role of the brain–gut axis in the development and progression of Alzheimer's disease

“…[ 4 ] The intestinal mucosa and the blood–brain barrier (BBB) allow the passage of some cytokines, neurotransmitters, and neurotoxic substances synthesized by the gut microbiota, which affects the functions of brain and gut. [ 5 ] Thus, BGA is regarded as a multifunctional complex network in which the central, peripheral, immune, and endocrine systems are all involved in its bidirectional regulation.…”

“…Gut microbial compositions of AD patients are characterized by high proinflammatory microbial levels and low distribution of anti-inflammatory microorganisms, which lead to local inflammation, increased gastrointestinal permeability, abnormal secretion of neurotoxic metabolites, and impairment of BBB function. [ 5 ] Additionally, high abundance of Bacillus subtilis , Streptococcus spp., Escherichia coli , and Staphylococcus aureus in AD patients is strongly associated with the production of Aβ and lipopolysaccharides (LPS). [ 5 , 6 ] Aβ oligomers are first found in the gastrointestinal tract and migrate bottom-up to the brain.…”

“…[ 5 ] Additionally, high abundance of Bacillus subtilis , Streptococcus spp., Escherichia coli , and Staphylococcus aureus in AD patients is strongly associated with the production of Aβ and lipopolysaccharides (LPS). [ 5 , 6 ] Aβ oligomers are first found in the gastrointestinal tract and migrate bottom-up to the brain. [ 5 , 6 ] Once Aβ is produced in the gut, it easily enters the systemic circulation and accumulates in the brain due to increased permeability of the intestinal wall.…”

“…[ 5 , 6 ] Aβ oligomers are first found in the gastrointestinal tract and migrate bottom-up to the brain. [ 5 , 6 ] Once Aβ is produced in the gut, it easily enters the systemic circulation and accumulates in the brain due to increased permeability of the intestinal wall. [ 7 ] The accumulation of Aβ produced by gut microbiota in the brain triggers many downstream events such as the activation of NF-kB and the upregulation of proinflammatory microRNA-34a, which in turn downregulates the expression of triggering receptor expressed on myeloid cells 2.…”

“…Stress and aging activate intestinal gliocytes and mast cells, thereby increasing the intestinal permeability and ultimately making it easier for bacteria to enter the gut epithelium and trigger an immune response in the gut mucosal layer. [ 5 ] The top-down regulation of BGA in the pathological state of AD leads to enhancement of intestinal permeability, activation of inflammatory response, and an increase in proinflammatory gut microbiota, further worsening the AD symptoms.…”