The possible role of antioxidant vitamin C in Alzheimer's disease treatment and prevention

Abstract

Oxidative stress is suggested to play a major role in the pathogenesis of Alzheimer's disease (AD). Among the antioxidants, vitamin C has been regarded as the most important one in neural tissue. It also decreases β-amyloid generation and acetylcholinesterase activity and prevents endothelial dysfunction by regulating nitric oxide, a newly discovered factor in the pathogenesis and progression of AD. However, clinical trials using antioxidants, including vitamin C, in patients with AD yielded equivocal results. The current article discusses the relevance of vitamin C in the cellular and molecular pathogenesis of AD and explores its therapeutic potential against this neurodegenerative disorder.

Figure 1.

Molecular structure of l-ascorbic acid (the monovalent anion) and dehydroascorbate (oxidation product by the loss of 2 electrons and a proton; adapted from Rice, 2000).

Figure 2.

The vitamin C regulation in the central nervous system (CNS). Vitamin C enters from the blood into cerebrospinal fluid (CSF) by sodium-dependent vitamin C transporter type 2 (SVCT2) in the choroid plexus, and extracellular fluid (ECF) by carrier-mediated uptake and simple diffusion across brain capillaries (adapted from Rice, 2000).