Inflammatory mechanisms are thought to contribute to lesion pathogenesis and neuronal cell death in Alzheimer’s disease. Transforming growth factor-β (TGF-β) plays a central role in the response of the brain to injury, and is increased in the brain in Alzheimer’s disease. In this study we determine whether expression of TGF-β is abnormal in the microvasculature in Alzheimer’s disease and whether TGF-β affects vascular production of pro-inflammatory cytokines, interleukin (IL)-1β, and tumor necrosis factor (TNF)-α. Microvessels isolated from the cortices of Alzheimer’s disease patients and age-matched controls are analyzed for microvessel-associated and released TGF-β. Results from Western blot analysis and enzyme-linked immunosorbent assay indicate a higher level of TGF-β in Alzheimer’s disease vessels compared to controls. To determine whether TGF-β affects vascular release of inflammatory factors, cultured brain endothelial cells are treated with TGF-β and levels of IL-1β and TNF-α determined. Both enzyme-linked immunosorbent assay and Western blot analyses show that untreated endothelial cells express little IL-1β or TNF-α, but incubation with TGF-β results in robust expression of these factors by brain endothelial cells. Our results suggest that vessel-derived TGF-β contributes to inflammatory processes in the Alzheimer brain.