Chronic melatonin therapy fails to alter amyloid burden or oxidative damage in old Tg2576 mice: Implications for clinical trials

Joseph Quinn, Doris Kulhanek, Jessica Nowlin, Richard Jones, Domenico Praticò, Joshua Rokach, Robert Stackman

Research output: Contribution to journalArticle

72 Scopus citations

Abstract

Melatonin has been proposed as a treatment for Alzheimer's disease based on the demonstration of antioxidant and "anti-amyloid" effects in vitro and in vivo. Chronic melatonin therapy in old, amyloid plaque-bearing transgenic mice was studied. Tg2576 mice started melatonin treatment at 14 months of age. After 4 months of treatment, there were no differences between untreated and melatonin-treated mice in cortical levels of soluble, formic acid extracted, or histologically detectable beta amyloid (Aβ), nor in brain levels of lipid peroxidation product (total 8,12-isoprostane F-VI), despite marked elevations in plasma melatonin. We conclude that melatonin fails to produce anti-amyloid or antioxidant effects when initiated after the age of amyloid plaque deposition. These findings diminish the possibility that melatonin will be useful for the treatment of established Alzheimer's disease.

Original languageEnglish (US)
Pages (from-to)209-213
Number of pages5
JournalBrain research
Volume1037
Issue number1-2
DOIs
StatePublished - Mar 10 2005

Keywords

  • Alzheimer's disease
  • Beta amyloid
  • Melatonin

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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