Microglia-mediated neurotoxicity: uncovering the molecular mechanisms
Identifieur interne : 000C60 ( Main/Corpus ); précédent : 000C59; suivant : 000C61Microglia-mediated neurotoxicity: uncovering the molecular mechanisms
Auteurs : Michelle L. Block ; Luigi Zecca ; Jau-Shyong HongSource :
- Nature Reviews Neuroscience [ 1471-003X ] ; 2007-01.
Abstract
Mounting evidence indicates that microglial activation contributes to neuronal damage in neurodegenerative diseases. Recent studies show that in response to certain environmental toxins and endogenous proteins, microglia can enter an overactivated state and release reactive oxygen species (ROS) that cause neurotoxicity. Pattern recognition receptors expressed on the microglial surface seem to be one of the primary, common pathways by which diverse toxin signals are transduced into ROS production. Overactivated microglia can be detected using imaging techniques and therefore this knowledge offers an opportunity not only for early diagnosis but, importantly, for the development of targeted anti-inflammatory therapies that might slow or halt the progression of neurodegenerative disease.
Url:
DOI: 10.1038/nrn2038
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ISTEX:2564A7978C41B9DFDA761DF190699894A3B9AF81Le document en format XML
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Block</name><affiliation><mods:affiliation>Neuropharmacology Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: Block@niehs.nih.gov</mods:affiliation></affiliation></author><author><name sortKey="Zecca, Luigi" sort="Zecca, Luigi" uniqKey="Zecca L" first="Luigi" last="Zecca">Luigi Zecca</name><affiliation><mods:affiliation>Institute of Biomedical Technologies, Italian National Research Council, 20090 Segrate (Milano), Italy.</mods:affiliation></affiliation></author><author><name sortKey="Hong, Jau Shyong" sort="Hong, Jau Shyong" uniqKey="Hong J" first="Jau-Shyong" last="Hong">Jau-Shyong Hong</name><affiliation><mods:affiliation>Neuropharmacology Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Nature Reviews Neuroscience</title><idno type="ISSN">1471-003X</idno><idno type="eISSN">1471-0048</idno><imprint><publisher>Nature Publishing Group</publisher><date type="published" when="2007-01">2007-01</date><biblScope unit="volume">8</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="57">57</biblScope><biblScope unit="page" to="69">69</biblScope></imprint><idno type="ISSN">1471-003X</idno></series><idno type="istex">2564A7978C41B9DFDA761DF190699894A3B9AF81</idno><idno type="DOI">10.1038/nrn2038</idno><idno type="ArticleID">nrn2038</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1471-003X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="eng">Mounting evidence indicates that microglial activation contributes to neuronal damage in neurodegenerative diseases. 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Her work focuses on Parkinson's disease; she investigates environmental and endogenous triggers of deleterious microglial activation and the molecular mechanisms driving the progressive and selective loss of dopaminergic neurons.</note><affiliation>Michelle Block is an Intramural Research Training Award fellow in the laboratory of Jau-Shyong Hong in the Laboratory of Pharmacology and Chemistry at the National Institute of Environmental Health Sciences at the National Institutes of Health, Research Triangle Park, North Carolina, USA. Her work focuses on Parkinson's disease; she investigates environmental and endogenous triggers of deleterious microglial activation and the molecular mechanisms driving the progressive and selective loss of dopaminergic neurons.</affiliation><affiliation>Neuropharmacology Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.</affiliation></author><author><persName><forename type="first">Luigi</forename><surname>Zecca</surname></persName><note type="biography">Luigi Zecca is head of the Neurodegenerative Diseases Unit at the Institute of Biomedical Technologies of the Italian National Research Council in Milano, Italy. His research interests are brain aging and neurodegenerative mechanisms of Parkinson's disease, with particular emphasis on the role of neuromelanin and metals, a field in which he has pioneered related studies. In particular, he described key aspects of the structure of neuromelanin, its synthesis, accumulation in aging, interaction with metals and role in neurodegeneration.</note><affiliation>Luigi Zecca is head of the Neurodegenerative Diseases Unit at the Institute of Biomedical Technologies of the Italian National Research Council in Milano, Italy. His research interests are brain aging and neurodegenerative mechanisms of Parkinson's disease, with particular emphasis on the role of neuromelanin and metals, a field in which he has pioneered related studies. In particular, he described key aspects of the structure of neuromelanin, its synthesis, accumulation in aging, interaction with metals and role in neurodegeneration.</affiliation><affiliation>Institute of Biomedical Technologies, Italian National Research Council, 20090 Segrate (Milano), Italy.</affiliation></author><author><persName><forename type="first">Jau-Shyong</forename><surname>Hong</surname></persName><note type="biography">Jau-Shyong Hong is the head of the Neuropharmacology Section in the Laboratory of Pharmacology and Chemistry at the National Institute of Environmental Health Sciences at the National Institutes of Health, Research Triangle Park, North Carolina, USA. His research interests focus on microglia-mediated neurotoxicity and the contribution of inflammation to Parkinson's disease and progressive neurotoxicity. Work from his laboratory has outlined vital mechanisms responsible for deleterious microglial activation and identified several novel therapeutic compounds that attenuate inflammation-mediated neurodegeneration.</note><affiliation>Jau-Shyong Hong is the head of the Neuropharmacology Section in the Laboratory of Pharmacology and Chemistry at the National Institute of Environmental Health Sciences at the National Institutes of Health, Research Triangle Park, North Carolina, USA. His research interests focus on microglia-mediated neurotoxicity and the contribution of inflammation to Parkinson's disease and progressive neurotoxicity. Work from his laboratory has outlined vital mechanisms responsible for deleterious microglial activation and identified several novel therapeutic compounds that attenuate inflammation-mediated neurodegeneration.</affiliation><affiliation>Neuropharmacology Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.</affiliation></author></analytic><monogr><title level="j">Nature Reviews Neuroscience</title><idno type="pISSN">1471-003X</idno><idno type="eISSN">1471-0048</idno><imprint><publisher>Nature Publishing Group</publisher><date type="published" when="2007-01"></date><biblScope unit="volume">8</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="57">57</biblScope><biblScope unit="page" to="69">69</biblScope></imprint></monogr><idno type="istex">2564A7978C41B9DFDA761DF190699894A3B9AF81</idno><idno type="DOI">10.1038/nrn2038</idno><idno type="ArticleID">nrn2038</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2007</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Mounting evidence indicates that microglial activation contributes to neuronal damage in neurodegenerative diseases. 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Work from his laboratory has outlined vital mechanisms responsible for deleterious microglial activation and identified several novel therapeutic compounds that attenuate inflammation-mediated neurodegeneration.</p></bio></au><aff><oid id="a1"></oid><org>Neuropharmacology Section, National Institute of Environmental Health Sciences</org>, <cty>Research Triangle Park</cty>, <st>North Carolina</st> <zip>27709</zip>, <cny>USA</cny>.</aff><aff><oid id="a2"></oid><org>Institute of Biomedical Technologies, Italian National Research Council</org>, <zip>20090</zip> <cty>Segrate (Milano)</cty>, <cny>Italy</cny>.</aff><caff><coid id="c1"></coid><email>Block@niehs.nih.gov</email></caff></aug><execsumm><p><list id="l1" type="bullet"><li>Unregulated microglial activation is a contributing mechanism of neuronal damage in neurodegenerative diseases.</li><li>Microglia continuously monitor the brain environment and are activated in response to diverse cues, including both endogenous proteins and externally derived environmental toxins.</li><li>Recent studies show that NADPH oxidase is a common mechanism of microglia-mediated neurotoxicity and is the primary source of microglia-derived extracellular reactive oxygen species (ROS) for numerous neurotoxic stimuli.</li><li>Pattern recognition receptors are a predominant mechanism through which microglia transduce diverse toxin signals into the production of ROS, identifying a common pathway of microglia-mediated neurotoxicity.</li><li>By using <i>in vivo</i> imaging to identify deleterious microglial activation combined with targeted anti-inflammatory therapy to inhibit the common neurotoxic mechanisms of microglial activation, it might be possible to slow or halt the progression of neurodegenerative disease.</li></list></p></execsumm><websumm>Microglial activation in response to environmental toxins or endogenous proteins might make a key contribution to neuronal damage after injury and in neurodegenerative diseases. Block and colleagues describe recent insights into the molecular mechanisms underlying the overactivation of microglia.</websumm><abs><p>Mounting evidence indicates that microglial activation contributes to neuronal damage in neurodegenerative diseases. Recent studies show that in response to certain environmental toxins and endogenous proteins, microglia can enter an overactivated state and release reactive oxygen species (ROS) that cause neurotoxicity. Pattern recognition receptors expressed on the microglial surface seem to be one of the primary, common pathways by which diverse toxin signals are transduced into ROS production. Overactivated microglia can be detected using imaging techniques and therefore this knowledge offers an opportunity not only for early diagnosis but, importantly, for the development of targeted anti-inflammatory therapies that might slow or halt the progression of neurodegenerative disease.</p></abs></fm></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="eng"><title>Microglia-mediated neurotoxicity: uncovering the molecular mechanisms</title></titleInfo><titleInfo type="alternative" lang="eng" contentType="CDATA"><title>Microglia-mediated neurotoxicity: uncovering the molecular mechanisms</title></titleInfo><name type="personal"><namePart type="given">Michelle L.</namePart><namePart type="family">Block</namePart><affiliation>Neuropharmacology Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.</affiliation><affiliation>E-mail: Block@niehs.nih.gov</affiliation><role><roleTerm type="text">author</roleTerm></role><description>Michelle Block is an Intramural Research Training Award fellow in the laboratory of Jau-Shyong Hong in the Laboratory of Pharmacology and Chemistry at the National Institute of Environmental Health Sciences at the National Institutes of Health, Research Triangle Park, North Carolina, USA. Her work focuses on Parkinson's disease; she investigates environmental and endogenous triggers of deleterious microglial activation and the molecular mechanisms driving the progressive and selective loss of dopaminergic neurons.</description></name><name type="personal"><namePart type="given">Luigi</namePart><namePart type="family">Zecca</namePart><affiliation>Institute of Biomedical Technologies, Italian National Research Council, 20090 Segrate (Milano), Italy.</affiliation><role><roleTerm type="text">author</roleTerm></role><description>Luigi Zecca is head of the Neurodegenerative Diseases Unit at the Institute of Biomedical Technologies of the Italian National Research Council in Milano, Italy. His research interests are brain aging and neurodegenerative mechanisms of Parkinson's disease, with particular emphasis on the role of neuromelanin and metals, a field in which he has pioneered related studies. 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