Melatonin in Alzheimer’s Disease
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 prote...
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doaj-54b3980fbe4a4c4eb27154d43f9bbbf82020-11-24T20:48:01ZengMDPI AGInternational Journal of Molecular Sciences1422-00672013-07-01147145751459310.3390/ijms140714575Melatonin in Alzheimer’s DiseaseJian-Zhi WangQing TianJiang ChuShu-Sheng YangQiong-Xia HuangLi LinAlzheimer’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.http://www.mdpi.com/1422-0067/14/7/14575Alzheimer’s diseasemelatonintau hyperphosphorylationbeta amyloidantioxidationcholinergicneuroinflammation |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Jian-Zhi Wang Qing Tian Jiang Chu Shu-Sheng Yang Qiong-Xia Huang Li Lin |
spellingShingle |
Jian-Zhi Wang Qing Tian Jiang Chu Shu-Sheng Yang Qiong-Xia Huang Li Lin Melatonin in Alzheimer’s Disease International Journal of Molecular Sciences Alzheimer’s disease melatonin tau hyperphosphorylation beta amyloid antioxidation cholinergic neuroinflammation |
author_facet |
Jian-Zhi Wang Qing Tian Jiang Chu Shu-Sheng Yang Qiong-Xia Huang Li Lin |
author_sort |
Jian-Zhi Wang |
title |
Melatonin in Alzheimer’s Disease |
title_short |
Melatonin in Alzheimer’s Disease |
title_full |
Melatonin in Alzheimer’s Disease |
title_fullStr |
Melatonin in Alzheimer’s Disease |
title_full_unstemmed |
Melatonin in Alzheimer’s Disease |
title_sort |
melatonin in alzheimer’s disease |
publisher |
MDPI AG |
series |
International Journal of Molecular Sciences |
issn |
1422-0067 |
publishDate |
2013-07-01 |
description |
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. |
topic |
Alzheimer’s disease melatonin tau hyperphosphorylation beta amyloid antioxidation cholinergic neuroinflammation |
url |
http://www.mdpi.com/1422-0067/14/7/14575 |
work_keys_str_mv |
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