Because of metabolic pathology, this chronic inflammatory state leads to a vicious cycle in which microglia, rather than removing pathology, become a site of neurotoxicity, generating pro-inflammatory cytokines (TNF-α, IL-1β) and further contributing to synaptic loss and neuronal damage, ultimately speeding up the progression of AD disease (Valiukas et al. 2025). This evidence concerns the gene IL1B and Alzheimer disease.