Beneficial effects of melatonin in experimental models of Alzheimer disease
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.
Keywords:
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.