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Int. J. Mol. Sci. 2013, 14(7), 14575-14593; doi:10.3390/ijms140714575

Melatonin in Alzheimer’s Disease

1,*  and 1,*
1 Key Laboratory of Neurological Disease of National Education Ministry and Hubei Province, Department of Pathology and Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China 2 Department of Pathology and Pathophysiology, College of Medical Science, Jishou University, 120 People Road, Jishou 436100, China 3 Department of TCM Rationale, College of Basic Medicine, Hubei University of Chinese Medicine, 1 West Road Huangjia Lake, Wuhan 430065, China These authors contributed equally to this work.
* Authors to whom correspondence should be addressed.
Received: 9 January 2013 / Revised: 21 June 2013 / Accepted: 5 July 2013 / Published: 12 July 2013
(This article belongs to the Section Molecular Pathology)
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Alzheimer’s disease (AD), an age-related neurodegenerative disorder with progressive cognition deficit, is characterized by extracellular senile plaques (SP) of aggregated β-amyloid (Aβ) and intracellular neurofibrillary tangles, mainly containing the hyperphosphorylated microtubule-associated protein tau. Multiple factors contribute to the etiology of AD in terms of initiation and progression. Melatonin is an endogenously produced hormone in the brain and decreases during aging and in patients with AD. Data from clinical trials indicate that melatonin supplementation improves sleep, ameliorates sundowning and slows down the progression of cognitive impairment in AD patients. Melatonin efficiently protects neuronal cells from Aβ-mediated toxicity via antioxidant and anti-amyloid properties. It not only inhibits Aβ generation, but also arrests the formation of amyloid fibrils by a structure-dependent interaction with Aβ. Our studies have demonstrated that melatonin efficiently attenuates Alzheimer-like tau hyperphosphorylation. Although the exact mechanism is still not fully understood, a direct regulatory influence of melatonin on the activities of protein kinases and protein phosphatases is proposed. Additionally, melatonin also plays a role in protecting the cholinergic system and in anti-inflammation. The aim of this review is to stimulate interest in melatonin as a potentially useful agent in the prevention and treatment of AD.
Keywords: Alzheimer’s disease; melatonin; tau hyperphosphorylation; beta amyloid; antioxidation; cholinergic; neuroinflammation Alzheimer’s disease; melatonin; tau hyperphosphorylation; beta amyloid; antioxidation; cholinergic; neuroinflammation
This is an open access article distributed under the Creative Commons Attribution License (CC BY) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Lin, L.; Huang, Q.-X.; Yang, S.-S.; Chu, J.; Wang, J.-Z.; Tian, Q. Melatonin in Alzheimer’s Disease. Int. J. Mol. Sci. 2013, 14, 14575-14593.

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