Abstract
This review article discusses the special role that melatonin, a molecule with
 chronobiotic/cytoprotective properties, may have in prevention and treatment of
 the metabolic syndrome (MS), ischemic and non-ischemic cardiovascular diseases
 and Alzheimer´s disease (AD). Prevention of these diseases is a major goal for
 governmental and non-governmental organizations, and melatonin, an unusual
 phylogenetically conserved molecule present in all aerobic organisms, merits
 consideration in this respect. In humans, circulating melatonin levels are consistently
 reduced in MS, ischemic and non-ischemic cardiovascular diseases and AD, the
 potential therapeutic value of melatonin being suggested by a limited number of
 clinical trials generally employing melatonin in the 2-5 mg/day range. In
 animal model studies of MS, ischemic and non-ischemic cardiovascular diseases
 and AD melatonin was very effective to curtail symptomatology. However,
 calculations derived from animal studies indicate projected cytoprotective
 melatonin doses for humans in the 40-100 mg/day range, doses that are rarely
 employed clinically. Hence, controlled studies employing melatonin doses in
 this range are urgently needed. Since the pharmaceutical industry is refractive
 to support them because of the lack of protective patents for a natural
 compound, only the involvement of governmental and non-profit organizations can
 achieve that goal. Within this prospect, the off-label use of melatonin is
 discussed.
Highlights
Chronic, endemic disorders such as the metabolic syndrome (MS) and Alzheimers disease (AD) are major health problems and their prevention is presently a fundamental goal for governmental and non-governmental organizations
In rats fed from weaning with a high-fat diet melatonin decreased body weight gain, feed efficiency and plasma glucose, leptin and triglyceride levels In high-fat diet-fed mice, melatonin improved insulin sensitivity and glucose tolerance
In 3.5 - 5.5 month–old APP/PS1 transgenic mice receiving melatonin or ramelteon for 5.5 months a significant reduction in hippocampal protein oxidation was observed In 11- 12-month-old APPsw mice treated with melatonin for 1 month a near complete restoration of brain mitochondrial function was found In 6-month-old 3xTg-AD mice treated with melatonin for 6 months both melatonin and physical exercise decreased soluble amyloid β oligomers, whereas only melatonin decreased hyperphosphorylated tau
Summary
Endemic disorders such as the metabolic syndrome (MS) and Alzheimers disease (AD) are major health problems and their prevention is presently a fundamental goal for governmental and non-governmental organizations. AD and related dementia are disorders characterized by a progressive deterioration of the structure and function of the brain, with symmetric losses of neurons in the cognitive, motor or sensory systems The regular intake of antioxidants has been recommended for prevention of neurodegenerative diseases in ageing, the effectiveness of this treatment has been discussed [7] In this context, the use of melatonin as a cytoprotective agent merits consideration.
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