Animal experiments have shown that chronic copper exposure increases the risk of the degenerative transformation of microglia and leads to accelerated cognitive decline in AD mice.[58] Also, 24-hour copper exposure inhibited phagocytosis or low-density lipoprotein receptor-related protein 1-dependent phagocytosis of mouse microglia, which attenuated Aβ clearance and caused increased release of pro-inflammatory cytokines such as IL-1β, TNF-α, and IL-6.[28] Microglia activation may be associated with copper-induced oxidative stress and activation of the NF-κB pathway. This evidence concerns the gene NFKB1 and Alzheimer disease.