• The effect of intestinal microbes in Alzheimer's disease
  • Maryam Rahbar sooreh,1 Saman Hakimian,2,*
    1. M.sc student of Microbiology ,Faculty of Basic Sciences , Islamic Azad University Urmia ,Iran , Tehran
    2. M.sc student of Microbiology, Islamic Azad University Central Tehran Branch ,Iran , Tehran


  • Introduction: Alzheimer's is a fatal degenerative brain disorder that leads to brain shrinkage and dementia. Alzheimer's disease is manifested by decreased levels of tau protein, hyperphosphorylation and accumulation of beta-amyloid peptide in the hippocampus and cingulate cortex. The nerve tissue of Alzheimer's patients contains fungal proteins that are associated with bacterial infections. Two methods of immunohistochemistry and next generation sequencing (NGS) were used to evaluate fungal and bacterial infections. The most common fungal species: Alternaria _ Candida _ Botris and Malassezia. Types of bacterial infection: Proteobacteria _ Actinobacteria _ Bacteroides Also, a sensitive cycle of uncontrolled neuroinflammation and neurodegeneration in the brain by herpes simplex virus type (HSV1)1. Systemic pro-inflammatory cytokines are produced by cytomegalovirus and Helicobacter pylori microorganisms. And then they can cross the blood and brain barrier and cause Alzheimer's disease. Inflammatory-activating gut bacteria release beta-amyloid protein and other neurotoxic substances. They can also secrete large amounts of amyloid and lyopolysaccharide. Bacteria produce endotoxin, which is usually found in the outer membrane of Gram-negative bacteria. During bacterial infection or changes in the metabolic processes of the intestinal microbiota due to inflammation, the concentration of LPS increases, which can cause neurodegeneration. Spirochetes contain amyloidogenic proteins and also induce beta amyloid deposition, tau protein phosphorylation, activate complement, affect vascular permeability, produce nitric oxide and free radicals, induce apoptosis. and are amyloidogens, which cause Alzheimer's disease.
  • Methods: Also microorganisms through the secretion of cortisol by the HPA in case of stress, which can affect intestinal motility, integrity, and mucus production, leading to changes in gut microbiota composition. This alteration, in turn, may affect the CNS through the modulation of stress hormones. Increased intestinal discomfort and altered BBB permeability cause microbiota dysbiosis, leading to the release of amyloids and lipopolysaccharides. This further modulates NF-κB signaling and a massive pro-inflammatory cytokine storm, causing neuronal loss.
  • Results: The mechanisms potentially involved in these processes as well as the potential of probiotics and prebiotics in therapeutic modulation of contributed pathways are discussed Through pro-inflammatory cytokines and chemokines.Immunity is also critically involved. Specifically, toll-like receptors (TLRs) and peptidoglycans (PGNs) mediate the immune response towards microbes by acting as sensors of microbial components. A local immune activation can, throughout different pathways, lead to an immune activation in different organs, including the brain. This low-grade immune activation has been implicated in the pathophysiology of some forms of depression and neurodegenerative disorders such as AD and Parkinson’s disease (PD).
  • Conclusion: It can be said Nutrition is known to play an important role in the pathogenesis of Alzheimer's disease. Evidence is obtained that the gut microbiota is a key player in these processes. Dietary changes (both adverse and beneficial) may influence the microbiome composition, thereby affecting the gut-brain axis and the subsequent risk for Alzheimer's disease progression. In this review, the research findings that support the role of intestinal microbiota in connection between nutritional factors and the risk for Alzheimer's disease onset and progression are summarized.
  • Keywords: Alzheimer's disease , microorganism , Gut microbiota ,