In a study on dementia-free subjects high levels of IL-1β and TNF-α were associated with an increased risk of developing Alzheimer’s disease [58], while the induction of Th2-biased responses seems to improve the clinical and pathophysiological condition in an Alzheimer’s mouse model, increasing IL-10 and reducing IFN-γ, TNF-α, IL-2 and IL-4 [176, 177]. This evidence concerns the gene IL4 and early-onset autosomal dominant Alzheimer disease.