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Chronic melatonin therapy fails to alter amyloid burden or oxidative damage in old Tg2576 mice: implications for
Joseph Quinn1, Doris Kulhanek, Jessica Nowlin
1Portland Veteran's Affairs Medical Center, Department of Neurology, Portland, OR 97239, USA. quinnj@ohsu.edu
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 (Abeta), nor in brain levels of lipid peroxidation product (total 8,12-isoprostane F(2alpha)-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.
Insights
Melatonin did not reduce amyloid plaques or oxidative stress in aged Alzheimer's model mice. This suggests melatonin is unlikely to treat established Alzheimer's disease.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Melatonin exhibits antioxidant and anti-amyloid properties in vitro and in vivo.
- Alzheimer's disease (AD) is characterized by amyloid plaque deposition and oxidative stress.
Purpose of the Study:
- To investigate the efficacy of chronic melatonin therapy in mitigating amyloid pathology and oxidative damage in aged, amyloid plaque-bearing transgenic mice.
Main Methods:
- Tg2576 mice, aged 14 months, received melatonin treatment for 4 months.
- Evaluated cortical levels of soluble, formic acid-extracted, and histological beta-amyloid (Abeta).
- Assessed brain levels of the lipid peroxidation product, 8,12-isoprostane F(2alpha)-VI.
Main Results:
- Melatonin treatment did not alter cortical Abeta levels (soluble, extracted, or detectable).
- No significant differences were observed in brain lipid peroxidation products between treated and untreated groups.
- Plasma melatonin levels were markedly elevated, indicating successful administration.
Conclusions:
- Melatonin therapy initiated after amyloid plaque deposition fails to demonstrate anti-amyloid or antioxidant effects in this Alzheimer's disease model.
- These findings suggest melatonin may not be a viable therapeutic option for established Alzheimer's disease.