Next Article in Journal
Integrated Self-Assembly of the Mms6 Magnetosome Protein to Form an Iron-Responsive Structure
Previous Article in Journal
Chemical and Colloidal Stability of Carboxylated Core-Shell Magnetite Nanoparticles Designed for Biomedical Applications
Open AccessReview

Melatonin in Alzheimer’s Disease

by 1,2,†, 3,†, 2, 1, 1,* and 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
Department of Pathology and Pathophysiology, College of Medical Science, Jishou University, 120 People Road, Jishou 436100, China
Department of TCM Rationale, College of Basic Medicine, Hubei University of Chinese Medicine, 1 West Road Huangjia Lake, Wuhan 430065, China
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2013, 14(7), 14575-14593;
Received: 9 January 2013 / Revised: 21 June 2013 / Accepted: 5 July 2013 / Published: 12 July 2013
(This article belongs to the Section Biochemistry)
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. View Full-Text
Keywords: Alzheimer’s disease; melatonin; tau hyperphosphorylation; beta amyloid; antioxidation; cholinergic; neuroinflammation Alzheimer’s disease; melatonin; tau hyperphosphorylation; beta amyloid; antioxidation; cholinergic; neuroinflammation
MDPI and ACS Style

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.

AMA Style

Lin L, Huang Q-X, Yang S-S, Chu J, Wang J-Z, Tian Q. Melatonin in Alzheimer’s Disease. International Journal of Molecular Sciences. 2013; 14(7):14575-14593.

Chicago/Turabian Style

Lin, Li; Huang, Qiong-Xia; Yang, Shu-Sheng; Chu, Jiang; Wang, Jian-Zhi; Tian, Qing. 2013. "Melatonin in Alzheimer’s Disease" Int. J. Mol. Sci. 14, no. 7: 14575-14593.

Find Other Styles

Article Access Map by Country/Region

Only visits after 24 November 2015 are recorded.
Search more from Scilit
Back to TopTop