Beneficial effects of melatonin in experimental models of Alzheimer disease1

Authors

  • Yong CHENG,

    1. Department of Pharmacology, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China
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  • Zheng FENG,

    1. Department of Anesthesiology, University of California, San Diego, and Veterans Affairs Medical Center, 3350 La Jolla Village Drive, San Diego, CA 92161, USA
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  • Qing-zhu ZHANG,

    1. Department of Pharmacology, College of Pharmacy, Shandong University, Jinan 250012, China
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  • Jun-tian ZHANG

    Corresponding author
    1. Department of Pharmacology, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China
      Correspondence to Prof Jun-tian ZHANG. Phn 86-10-6316-5179. Fax 86-10-6316-5211. Ez-mail zhangjt@imm.ac.cn
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  • 1

    Project supported by a grant from the National Basic Research Program of the Ministry of Science and Technology, China (No G199805119).

Correspondence to Prof Jun-tian ZHANG. Phn 86-10-6316-5179. Fax 86-10-6316-5211. Ez-mail zhangjt@imm.ac.cn

Abstract

Alzheimer's disease (AD), a progressive degenerative disorder, is characterized by the presence of amyloid deposits, neurofibrillary tangles and neuron loss. Emerging evidence indicates that antioxidants could be useful either for the prevention or treatment of AD. It has been shown that melatonin is a potent antioxidant and free radical scavenger. Additionally, melatonin stimulates several antioxidative enzymes and improves mitochondrial energy metabolism. These findings led us to study amyloid precursor protein transgenic mice, ovariectomized rats, and pheochromocytoma and astroglioma cell lines, to observe whether melatonin had any effect on Alzheimer's symptoms or pathological changes. We found that melatonin had many beneficial effects in experimental models of AD, including improvement of cognitive function, anti-oxidative injury, anti-apoptosis, inhibition of β-amyloid (Aβ) deposition and Aβ fiber formation. Several groups have shown that melatonin has an inhibitory effect on tau protein hyperphosphorylation. These actions may potentially slow down or stop the progression of dementia.

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