This suggests that the production of TNFα and IL-1β is an early and relatively transient process, rather than a prolonged and stable event, such as glial activation in the AD brain, because pathological alterations, including Aβ accumulation and glial activation, were first detected in the cortex of 5XFAD mice (Oakley et al., 2006). This evidence concerns the gene IL1B and Alzheimer disease.