#Cardinal chains lvl 74 free#
This concept is based on the free radical hypothesis of aging as proposed by Harman more than 50 years ago. Oxidative damage has been suggested as the primary cause of aging and age-associated neurodegenerative diseases like Alzheimer’s disease (AD). clinical and subjective relevance) before melatonin´s use can be advocated. In the case of AD, larger randomized controlled trials are necessary to yield evidence of effectiveness (i.e. The analysis of published evidence made it possible to postulate melatonin as a useful ad-on therapeutic tool in MCI. Only clinical studies with empirical treatment data were reviewed. Full publications were obtained and references were checked for additional material where appropriate. Search terms were “Alzheimer” and “melatonin”. PubMed was searched using Entrez for articles including clinical trials and published up to 15 January 2010. The aim of this manuscript was to assess published evidence of the efficacy of melatonin to treat AD and MCI patients. This is of particularly importance in mild cognitive impairment (MCI), an etiologically heterogeneous syndrome that precedes dementia. The antioxidant, mitochondrial and antiamyloidogenic effects of melatonin indicate its potentiality to interfere with the onset of the disease. Melatonin replacement has been shown effective to treat sundowning and other sleep wake disorders in AD patients. Half of severely ill AD patients develop chronobiological day-night rhythm disturbances like an agitated behavior during the evening hours (so-called “sundowning”). Melatonin secretion decreases in Alzheimer´s disease (AD) and this decrease has been postulated as responsible for the circadian disorganization, decrease in sleep efficiency and impaired cognitive function seen in those patients.
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