Abstract

Alzheimer’s disease (AD) is the most common cause of dementia in older people. Acetylcholinesterase inhibitors and memantine are licensed for AD and have moderate symptomatic benefi ts. Although the initiating events are yet unknown, it is clear that AD, at least its sporadic form, results from a combination of genetic risk factors and different epigenetic events. Among them, a growing body of evidence suggests that an imbalance between free radical formation and destruction is involved in AD pathogenesis. Exogenous antioxidant supplementation,  supposedly, could play a role in AD, combating oxidative damage and compensating for the decreased level of endogenous antioxidants.
Although epidemiologic studies show that dietary intake of antioxidants reduces the risk of AD, clinical trials with antioxidants show only a marginal positive or zero effect (i.e. ginkgo biloba, melatonin, lipoeic acid, tocoferol). Development of antioxidative drugs for treatment of AD can break the vicious cycle of oxidative stress and neurodegeneration offering new opportunities in prevention and treatment of AD.