More and more studies have reported that β-amyloid (Aβ)-induced oxidative stress and protein metabolism disorders along with their interactions are likely to be the key factors to the pathogenesis of Alzheimers disease (AD). Heme oxygenase (HO) is one member of stress responsive enzyme super family and is a joint of many hypothesis for AD, while oxidative stress, iron metabolism disorders and Aβ deposition are closely related with HO. Therefore, HO is expected to become a therapeutic target for AD. HO-1 and HO-2 are the main members of HO family, and keep dynamic balance. In normal aging brain tissues, the expression of HO-2 is high, and that of HO-1 is low; while in the cerebral cortex and hippocampus of AD patients, the expression of HO-1 is significantly increased. This phenomenon indicates that HO-1 has a protective effect to the neurons from the oxidative stress. Furthermore, heme and Aβ could form Aβ-heme compound, which is a peroxidase complex, which increase the oxidative damage to neurons. Recently, Curcumin has been shown cytoprotective properties by inducing HO-1 and by preventing the formation of Aβ-heme in neurons; however, the underlying mechanisms are still unclear to date. Therefore, there has been great interest in understanding the molecular mechanisms based on curcumin acts on.