Melatonin as a pharmacological agent against neuronal loss in experimental models of Huntington's disease, Alzheimer's disease and Parkinsonism

Russel J. Reiter, Javier Cabrera, Rosa M. Sainz, Juan Carlos Mayo, Lucien C. Manchester, Dun Xian Tan

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Abstract

This review summarizes the experimental findings related to the neuroprotective role of melatonin. In particular, it focuses on research directed at models of Huntington's disease, Alzheimer's disease and Parkinsonism. Melatonin has been shown to be highly effective in reducing oxidative damage in the central nervous system; this efficacy derives from its ability to directly scavenge a number of free radicals and to function as an indirect antioxidant. In particular, melatonin detoxifies the highly toxic hydroxyl radical as well as the peroxyl radical, peroxynitrite anion, nitric oxide, and singlet oxygen, all of which can damage macromolecules in brain cells. Additionally, melatonin stimulates a variety of antioxidative enzymes including superoxide dismutase, glutathione peroxidase and glutathione reductase. One additional advantage melatonin has in reducing oxidative damage in the central nervous system is the ease with which to crosses the blood-brain barrier. This combination of actions makes melatonin a highly effective pharmacological agent against free radical damage. The role of physiological levels of melatonin in forestalling oxidative damage in the brain is currently being tested.

Original languageEnglish (US)
Pages (from-to)471-485
Number of pages15
JournalAnnals of the New York Academy of Sciences
Volume890
DOIs
StatePublished - Jan 1 1999

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ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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