Molecular links between inflammatory bowel disease and Alzheimer’s disease through immune signaling and inflammatory pathways

Figure 4 Gut-brain axis: From dysbiosis to neuroinflammation. Gut dysbiosis leads to a leaky gut and systemic inflammation, releasing pro-inflammatory mediators. These mediators cross a compromised blood-brain barrier, activating resting microglia into a pro-inflammatory M1 phenotype. Activated M1 microglia release cytokines, chemokines, and reactive oxygen species, causing neuronal damage (dystrophic neurons) and contributing to pathologies like amyloid-β plaque formation and microgliosis, highlighting the gut-brain axis's role in neuroinflammation. LPS: Lipopolysaccharides; TLRs: Toll-like receptors; TNF-α: Tumor necrosis factor-alpha; IL: Interleukin; BBB: Blood-brain barrier; TREM2: Triggering receptor expressed on myeloid cells 2; NF-kB: Nuclear factor kappa B; ROS: Reactive oxygen species.