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      Melatonin Regulates Aging and Neurodegeneration through Energy Metabolism, Epigenetics, Autophagy and Circadian Rhythm Pathways

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          Abstract

          Brain aging is linked to certain types of neurodegenerative diseases and identifying new therapeutic targets has become critical. Melatonin, a pineal hormone, associates with molecules and signaling pathways that sense and influence energy metabolism, autophagy, and circadian rhythms, including insulin-like growth factor 1 (IGF-1), Forkhead box O (FoxOs), sirtuins and mammalian target of rapamycin (mTOR) signaling pathways. This review summarizes the current understanding of how melatonin, together with molecular, cellular and systemic energy metabolisms, regulates epigenetic processes in the neurons. This information will lead to a greater understanding of molecular epigenetic aging of the brain and anti-aging mechanisms to increase lifespan under healthy conditions.

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          The orphan nuclear receptor REV-ERBalpha controls circadian transcription within the positive limb of the mammalian circadian oscillator.

          Nicolas Preitner, Francesca Damiola, Luis-Lopez-Molina … (2002)
          Mammalian circadian rhythms are generated by a feedback loop in which BMAL1 and CLOCK, players of the positive limb, activate transcription of the cryptochrome and period genes, components of the negative limb. Bmal1 and Per transcription cycles display nearly opposite phases and are thus governed by different mechanisms. Here, we identify the orphan nuclear receptor REV-ERBalpha as the major regulator of cyclic Bmal1 transcription. Circadian Rev-erbalpha expression is controlled by components of the general feedback loop. Thus, REV-ERBalpha constitutes a molecular link through which components of the negative limb drive antiphasic expression of components of the positive limb. While REV-ERBalpha influences the period length and affects the phase-shifting properties of the clock, it is not required for circadian rhythm generation.
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            Regulation of yeast replicative life span by TOR and Sch9 in response to nutrients.

            M Kaeberlein (2005)
            Calorie restriction increases life span in many organisms, including the budding yeast Saccharomyces cerevisiae. From a large-scale analysis of 564 single-gene-deletion strains of yeast, we identified 10 gene deletions that increase replicative life span. Six of these correspond to genes encoding components of the nutrient-responsive TOR and Sch9 pathways. Calorie restriction of tor1D or sch9D cells failed to further increase life span and, like calorie restriction, deletion of either SCH9 or TOR1 increased life span independent of the Sir2 histone deacetylase. We propose that the TOR and Sch9 kinases define a primary conduit through which excess nutrient intake limits longevity in yeast.
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              Early aging and age-related pathologies in mice deficient in BMAL1, the core componentof the circadian clock.

              Roman Kondratov, Anna A Kondratova, Victoria Gorbacheva … (2006)
              Mice deficient in the circadian transcription factor BMAL1 (brain and muscle ARNT-like protein) have impaired circadian behavior and demonstrate loss of rhythmicity in the expression of target genes. Here we report that Bmal1(-/-) mice have reduced lifespans and display various symptoms of premature aging including sarcopenia, cataracts, less subcutaneous fat, organ shrinkage, and others. The early aging phenotype correlates with increased levels of reactive oxygen species in some tissues of the Bmal1(-/- )animals. These findings, together with data on CLOCK/BMAL1-dependent control of stress responses, may provide a mechanistic explanation for the early onset of age-related pathologies in the absence of BMAL1.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 22 September 2014
                Publication date Collection: September 2014
                Volume: 15
                Issue: 9
                Pages: 16848-16884
                Affiliations
                [1 ]Research Center for Neuroscience, Institute of Molecular Biosciences, Mahidol University, Salaya, Nakornpathom 73170, Thailand; E-Mails: anorutj@ 123456gmail.com (A.J.); chukorn.nop@ 123456mahidol.ac.th (C.N.); sujira.muk@ 123456mahidol.ac.th (S.M.)
                [2 ]Center for Innovation Development and Technology Transfer, Faculty of Medical Technology, Mahidol University, Salaya, Nakornpathom 73170, Thailand; E-Mail: prapimpun.won@ 123456mahidol.ac.th
                [3 ]Center for Neuroscience and Department of Pharmacology, Faculty of Science, Mahidol University, Rama VI Road, Bangkok 10400, Thailand
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: piyarat.gov@ 123456mahidol.ac.th ; Tel./Fax: +662-441-9003 (ext. 1311).
                Article
                Publisher ID: ijms-15-16848
                DOI: 10.3390/ijms150916848
                PMC ID: 4200827
                PubMed ID: 25247581
                SO-VID: 6cc098d9-edc3-4702-87bb-691a6fd714ae
                Copyright © © 2014 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 25 July 2014
                Date revision received : 03 September 2014
                Date accepted : 12 September 2014
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: melatonin,brain aging,energy metabolism,epigenetics,autophagy,circadian rhythm,neurodegeneration,sirtuins
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: melatonin, brain aging, energy metabolism, epigenetics, autophagy, circadian rhythm, neurodegeneration, sirtuins

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