Journal of Molecular Neuroscience

, Volume 21, Issue 1, pp 1–11

Antioxidant treatment in alzheimer’s disease

Current state
Review Article

DOI: 10.1385/JMN:21:1:1

Cite this article as:
Gilgun-Sherki, Y., Melamed, E. & Offen, D. J Mol Neurosci (2003) 21: 1. doi:10.1385/JMN:21:1:1

Abstract

Accumulating data from experimental and human studies indicate that oxidative stress (OS) plays a major role in the pathogenesis of Alzheimer’s disease (AD). The production of reactive oxygen species (ROS), which leads to OS, can occur very early, even before the appearance of symptoms and molecular events (β-amyloid plaques and neurofibrillary tangles), leading to tissue damage via several different cellular molecular pathways. ROS can cause damage to cardinal cellular components such as lipids, proteins, and nucleic acids (e.g., RNA, DNA), causing cell death by modes of necrosis or apoptosis. The damage can become more widespread because of the weakened cellular antioxidant defense systems. Therefore, treatment with antioxidants might theoretically act to prevent propagation of tissue damage and improve both survival and neurological outcome. Indeed, several studies preformed to date examined whether dietary intake of several antioxidants, mainly vitamins, might prevent or reduce the progression of AD. Although a few of the antioxidants showed some efficacy in these trials, no answer is yet available as to whether antioxidants are truly protective against AD. Reasons for these results might include, in part, blood-brain barrier (BBB) permeability, inappropriate timing of administration, or suboptimal drug levels at the target site in the central nervous system. Thus, antioxidant cocktails or antioxidants combined with other drugs may have more successful synergistic effects. Further, well-designed intervention, as well as observational investigations based on large cohorts studied over a long period of time with several methods for assessing antioxidant exposure, including relation to BBB penetration, are needed to test this hypothesis.

Index Entries

Alzheimer’s disease (AD) reactive oxygen species (ROS) oxygen stress (OS) antioxidants blood brain barrier (BBB) 

Copyright information

© Humana Press Inc 2003

Authors and Affiliations

  • Yossi Gilgun-Sherki
    • 1
  • Eldad Melamed
    • 1
  • Daniel Offen
    • 1
  1. 1.Laboratory of Neurosciences, Felsenstein Medical Research Center and Department of Neurology, Rabin Medical Center-Beilinson Campus, The Sackler School of MedicineTel Aviv UniversityPetach TikvaIsrael

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