It is possible that the age-dependent progressive increases in brain oxidative stress contributes or facilitates AD lesions. This hypothesis would indicate the convenience of effective measures to prevent and treat brain oxidative stress. However, until now, there have not been conclusive studies demonstrating efficacy of vitamin C and E in arresting or significantly delaying the onset of AD. More recently, the use of agents capable of crossing the blood-brain barrier, such as lipoic or dehydroascorbic acids, has been suggested (Harman, 2006). There is a large list of antioxidant compounds that have been suggested as beneficial to prevent or delay AD including defined chemical entities or natural products such as green tea, ginkgo biloba, red wine, blueberries, etc. Some effort is being made to define the efficacy of defined extracts (e.g., from blueberries or spinach) and of assessing their effects in suitable cell and animal models (Joseph, Shukitt-Hale, & Casadesus, 2005). Although there are some uncertainties, oxidative stress is no doubt a component of the AD pathology, the study of which might lead to suitable main or adjunct therapies in AD. The brain sources of oxidative agents, their contribution to neurodegeneration, and the potential applications of antioxidants in AD therapy are discussed by George Perry's laboratory in the chapter authored by Moreira and collaborators.
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