Open AccessBeneficial effects of melatonin in experimental models of Alzheimer disease 1
Author(s) -
CHENG Yong,
FENG Zheng,
ZHANG Qingzhu,
ZHANG Juntian
Publication year - 2006
Publication title -
acta pharmacologica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.514
H-Index - 90
eISSN - 1745-7254
pISSN - 1671-4083
DOI - 10.1111/j.1745-7254.2006.00267.x
Subject(s) - melatonin , free radical scavenger , medicine , hyperphosphorylation , endocrinology , antioxidant , oxidative stress , alzheimer's disease , neuroprotection , genetically modified mouse , mitochondrion , tau protein , chemistry , biology , transgene , disease , microbiology and biotechnology , biochemistry , kinase , gene
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.