infection contributes to the expression of Alzheimer's disease-associated risk factors and neuroinflammation.

Over time, mounting evidence has demonstrated extra-gastric manifestations of infection. As such, a number of studies demonstrated the potential contribution of infection to the incidence and progression of Alzheimer's disease (AD). Considering unanswered questions regarding the effect of infection on brain activity, we sought to investigate the impact of infection on the expression of AD-associated risk factors. We used two clinical strains obtained from two patients with peptic ulcer and evaluated their influence on the expression level of AD-associated genes (, , , , , , ) and genes for inflammatory markers (TLR-4, IL-8, TNF-α) by RT-qPCR in human glioblastoma (U87MG) and astrocyte (1321N1) cell lines. The expression of inflammatory cytokines was further assessed by ELISA assay. The exposure of U97MG and 1321N1 cells to strains resulted in a significant enhancement in the expression level of the risk allele , while reducing the expression of the protective allele . infection remarkably increased the expression level of main AD-associated risk genes, and also pro-inflammatory cytokines. Furthermore, we noticed a substantial elevation in the mRNA expression level of transmembrane receptor TLR-4 following infection. Our findings presented the potential for to stimulate the expression of AD-associated risk genes and trigger neuroinflammation in the brain tissue. This, in principle, leads to the recommendation that AD patients should perhaps test for infection and receive treatments upon positive detection.