Pioglitazone and 15d-prostaglandin J2 significantly reduced the infarct volume, attenuated the aggregation of parenchymal neutrophils, decreased the release of TNF-α, IL-1β, and IL-6, and improved neurological function in the cerebral ischemia injury mice [87, 88]; reduced β-amyloid levels effectively reversed cerebrovascular damage, improved energy metabolism and antioxidant capacity of model mice's cortex, and inhibited β-amyloid-stimulated COX-2, TNF-α, and IL-6 expression in Alzheimer's disease models [89–91]. Here, TNF is linked to early-onset autosomal dominant Alzheimer disease.