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      Therapeutic promise and principles : Metabotropic glutamate receptors

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          Abstract

          For a number of disease entities, oxidative stress becomes a significant factor in the etiology and progression of cell dysfunction and injury. Therapeutic strategies that can identify novel signal transduction pathways to ameliorate the toxic effects of oxidative stress may lead to new avenues of treatment for a spectrum of disorders that include diabetes, Alzheimer's disease, Parkinson's disease and immune system dysfunction. In this respect, metabotropic glutamate receptors (mGluRs) may offer exciting prospects for several disorders since these receptors can limit or prevent apoptotic cell injury as well as impact upon cellular development and function. Yet the role of mGluRs is complex in nature and may require specific mGluR modulation for a particular disease entity to maximize clinical efficacy and limit potential disability. Here we discuss the potential clinical translation of mGluRs and highlight the role of novel signal transduction pathways in the metabotropic glutamate system that may be vital for the clinical utility of mGluRs.

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          Global prevalence of diabetes: estimates for the year 2000 and projections for 2030.

          Sarah E Wild, Gojka Roglic, Anders Green … (2004)
          The goal of this study was to estimate the prevalence of diabetes and the number of people of all ages with diabetes for years 2000 and 2030. Data on diabetes prevalence by age and sex from a limited number of countries were extrapolated to all 191 World Health Organization member states and applied to United Nations' population estimates for 2000 and 2030. Urban and rural populations were considered separately for developing countries. The prevalence of diabetes for all age-groups worldwide was estimated to be 2.8% in 2000 and 4.4% in 2030. The total number of people with diabetes is projected to rise from 171 million in 2000 to 366 million in 2030. The prevalence of diabetes is higher in men than women, but there are more women with diabetes than men. The urban population in developing countries is projected to double between 2000 and 2030. The most important demographic change to diabetes prevalence across the world appears to be the increase in the proportion of people >65 years of age. These findings indicate that the "diabetes epidemic" will continue even if levels of obesity remain constant. Given the increasing prevalence of obesity, it is likely that these figures provide an underestimate of future diabetes prevalence.
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            Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade.

            P. Li, D Nijhawan, I Budihardjo … (1997)
            We report here the purification of the third protein factor, Apaf-3, that participates in caspase-3 activation in vitro. Apaf-3 was identified as a member of the caspase family, caspase-9. Caspase-9 and Apaf-1 bind to each other via their respective NH2-terminal CED-3 homologous domains in the presence of cytochrome c and dATP, an event that leads to caspase-9 activation. Activated caspase-9 in turn cleaves and activates caspase-3. Depletion of caspase-9 from S-100 extracts diminished caspase-3 activation. Mutation of the active site of caspase-9 attenuated the activation of caspase-3 and cellular apoptotic response in vivo, indicating that caspase-9 is the most upstream member of the apoptotic protease cascade that is triggered by cytochrome c and dATP.
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              Trends in oxidative aging theories.

              Florian Muller, Michael S Lustgarten, Youngmok Charles Jang … (2007)
              The early observations on the rate-of-living theory by Max Rubner and the report by Gershman that oxygen free radicals exist in vivo culminated in the seminal proposal in the 1950s by Denham Harman that reactive oxygen species are a cause of aging (free radical theory of aging). The goal of this review is to analyze recent findings relevant in evaluating Harman's theory using experimental results as grouped by model organisms (i.e., invertebrate models and mice). In this regard, we have focused primarily on recent work involving genetic manipulations. Because the free radical theory of aging is not the only theorem proposed to explain the mechanism(s) involved in aging at the molecular level, we also discuss how this theory is related to other areas of research in biogerontology, specifically, telomere/cell senescence, genomic instability, and the mitochondrial hypothesis of aging. We also discuss where we think the free radical theory is headed. It is now possible to give at least a partial answer to the question whether oxidative stress determines life span as Harman posed so long ago. Based on studies to date, we argue that a tentative case for oxidative stress as a life-span determinant can be made in Drosophila melanogaster. Studies in mice argue for a role of oxidative stress in age-related disease, especially cancer; however, with regard to aging per se, the data either do not support or remain inconclusive on whether oxidative stress determines life span.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oxid Med Cell Longev
                Journal ID (publisher-id): OMCL
                Title: Oxidative Medicine and Cellular Longevity
                Publisher: Landes Bioscience
                ISSN (Print): 1942-0900
                ISSN (Electronic): 1942-0994
                Publication date (Print): Oct-Dec 2008
                Volume: 1
                Issue: 1
                Pages: 1-14
                Affiliations
                [1 ]Division of Cellular and Molecular Cerebral Ischemia
                [2 ]Departments of Neurology and Anatomy & Cell Biology; 3Barbara Ann Karmanos Cancer Institute; 4Center for Molecular Medicine and Genetics; 5Institute of Environmental Health Sciences; Wayne State University School of Medicine; Detroit, Michigan USA
                Author notes
                Correspondence to: Kenneth Maiese, M.D.; Department of Neurology, 8C-1 UHC; Wayne State University School of Medicine; 4201 St. Antoine; Detroit, Michigan 48201 USA; Fax: 313.966.0486; Email: kmaiese@ 123456med.wayne.edu , aa2088@ 123456wayne.edu
                Article
                Publisher ID: 1942-0900-1-1-1
                PMC ID: 2740993
                PubMed ID: 19750024
                SO-VID: 57832f0e-9f5c-40f3-9eef-19a179f0a719
                Copyright © Copyright © 2008 Landes Bioscience
                History
                Date received : 21 August 2008
                Date revision received : 26 August 2008
                Date accepted : 27 August 2008
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular medicine
                Keywords: oxidative stress,wnt,forkhead,amyotrophic lateral sclerosis,alzheimer's disease,β-catenin,apoptosis,huntington's disease,erythropoietin,akt,metabotropic
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: oxidative stress, wnt, forkhead, amyotrophic lateral sclerosis, alzheimer's disease, β-catenin, apoptosis, huntington's disease, erythropoietin, akt, metabotropic

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