04-15-2008, 10:56 AM
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Lecturer
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Join Date: Apr 2006
Posts: 783
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Quote:
Originally Posted by Harry Hirsute
I can't copy-and-paste from the PDF source material.
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Harry, you click the "T" at the top of your PDF page, to enable 'cut & paste'.
Quote:
"Possible Therapeutic Value of Melatonin in Mild Cognitive Impairment: A Retrospective Study,"
Journal of Pineal Research, 2007; 43(4): 404-409. 45955 (3/2008)
Kirk Hamilton: Can you please share with us your educational background and current position?
Daniel P. Cardinali: I earned my M.D. and Ph.D. degrees from the Salvador University, Buenos Aires. I am
presently Professor of Physiology and Director of the Neuroscience Laboratory, Faculty of Medicine,
University of Buenos Aires.
KH: What got you interested in studying the role of melatonin and cognitive impairment?
DPC: My field of interest includes the physiology and pharmacology of the pineal gland and melatonin and
physiology and pharmacology of the biologic rhythms. Since 1968 I have worked on several aspects of
melatonin biology, describing its brain receptors in 1979 and several aspects of its mechanism of action in brain.
In recent years, and do to the fact that melatonin has been approved as a medication in Argentina, I have
examined the efficacy of melatonin for treatment of chronobiological disorders in Alzheimers disease.
KH: What is the mechanism of how melatonin might improve cognitive impairment?
DPC: Increased oxidative stress and mitochondrial dysfunction have been identified as common
pathophysiological phenomena associated with neurodegenerative disorders such as Alzheimer�s disease. As the
production of melatonin declines with age, it may contribute to increased levels of oxidative stress in the
elderly. Melatonin has multiple actions such as being a regulator of antioxidant and prooxidant enzymes, a free
radical scavenger and antagonist of mitochondrial radical formation. The ability of melatonin and its
kynuramine metabolites to interact directly with the electron transport chain by increasing the electron flow and
reducing electron leakage are unique features by which melatonin is able to increase the survival of neurons
under enhanced oxidative stress. Moreover, antifibrillogenic actions have been demonstrated in vitro, also in the
presence of profibrillogenic apoE4 or apoE3, and in vivo, in a transgenic mouse model. Amyloid-beta toxicity is
antagonized by melatonin and is one of its kynuramine metabolites. Cytoskeletal disorganization and protein
hyperphosphorylation, as induced in several cell-line models, have been attenuated by melatonin, its effects
comprising of stress kinase down-regulation and extending to neurotrophin expression. Various experimental
models of Alzheimers disease indicate the usefulness of melatonin in antagonizing disease progression and/or
mitigating some of the symptoms. Melatonin secretion has been found to be altered in Alzheimers disease.
Attempts to compensate for age- and disease-dependent melatonin deficiency have shown that administration of
this compound can improve sleep efficiency and to some extent, cognitive function in AD patients. Exogenous
melatonin has also been reported to alleviate behavioral symptoms such as sundowning.
KH: Is there away to assess for melatonin status in patients in general? By saliva, urine or serum? Were any
of these patients assessed for melatonin status?
DPC: The best way to assess melatonin secretion by the pineal gland is through the integrated 24 h urine
production of 6-sulfatoxymelatonin, the main metabolite of circulating melatonin. It must be noted, however,
that the levels of a lipophilic substance like melatonin reaching neurons under physiological or pharmacological
conditions can differ considerably from circulating hormone concentrations. Two compartments of melatonin
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https://www.vitasearch.com/get/PC/exp...AT01-16-08.pdf
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