The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases
Identifieur interne : 002967 ( Istex/Corpus ); précédent : 002966; suivant : 002968The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases
Auteurs : Patrick L. Mcgeer ; Edith G. McgeerSource :
- Brain Research Reviews [ 0165-0173 ] ; 1996.
Abstract
Cultured brain cells are capable of generating many molecules associated with inflammatory and immune functions. They constitute the endogenous immune response system of brain. They include complement proteins and their regulators, inflammatory cytokines, acute phase reactants and many proteases and protease inhibitors. Most of the proteins are made by microglia and astrocytes, but even neurons are producers. Many appear in association with Alzheimer disease lesions, indicating a state of chronic inflammation in Alzheimer disease brain. Such a state can apparently exist without stimulation by peripheral inflammatory mediators or the peripheral immune system. A strong inflammatory response may be autotoxic to neurons, exacerbating the fundamental pathology in Alzheimer disease and perhaps other neurological disorders. Autotoxic processes may contribute to cellular death in chronic inflammatory diseases affecting other parts of the body, suggesting the general therapeutic value of anti-inflammatory agents. With respect to Alzheimer disease, multiple epidemiological studies indicate that patients taking anti-inflammatory drugs or suffering from conditions in which such drugs are routinely used, have a decreased risk of developing Alzheimer disease. In one very preliminary clinical trial, the anti-inflammatory drug indomethacin arrested progress of the disease. New agents directed against the inflammatory processes revealed in studies of Alzheimer disease lesions may have broad therapeutic applications.
Url:
DOI: 10.1016/0165-0173(95)00011-9
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Mcgeer</name><affiliation><mods:affiliation>Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., V6T 1Z3, Canada</mods:affiliation></affiliation></author><author><name sortKey="Mcgeer, Edith G" sort="Mcgeer, Edith G" uniqKey="Mcgeer E" first="Edith G." last="Mcgeer">Edith G. Mcgeer</name><affiliation><mods:affiliation>Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., V6T 1Z3, Canada</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain Research Reviews</title><title level="j" type="abbrev">BRESR</title><idno type="ISSN">0165-0173</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1996">1996</date><biblScope unit="volume">21</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="195">195</biblScope><biblScope unit="page" to="218">218</biblScope></imprint><idno type="ISSN">0165-0173</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0165-0173</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cultured brain cells are capable of generating many molecules associated with inflammatory and immune functions. They constitute the endogenous immune response system of brain. They include complement proteins and their regulators, inflammatory cytokines, acute phase reactants and many proteases and protease inhibitors. Most of the proteins are made by microglia and astrocytes, but even neurons are producers. Many appear in association with Alzheimer disease lesions, indicating a state of chronic inflammation in Alzheimer disease brain. Such a state can apparently exist without stimulation by peripheral inflammatory mediators or the peripheral immune system. A strong inflammatory response may be autotoxic to neurons, exacerbating the fundamental pathology in Alzheimer disease and perhaps other neurological disorders. Autotoxic processes may contribute to cellular death in chronic inflammatory diseases affecting other parts of the body, suggesting the general therapeutic value of anti-inflammatory agents. With respect to Alzheimer disease, multiple epidemiological studies indicate that patients taking anti-inflammatory drugs or suffering from conditions in which such drugs are routinely used, have a decreased risk of developing Alzheimer disease. In one very preliminary clinical trial, the anti-inflammatory drug indomethacin arrested progress of the disease. New agents directed against the inflammatory processes revealed in studies of Alzheimer disease lesions may have broad therapeutic applications.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Patrick L. McGeer</name><affiliations><json:string>Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., V6T 1Z3, Canada</json:string></affiliations></json:item><json:item><name>Edith G. 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They constitute the endogenous immune response system of brain. They include complement proteins and their regulators, inflammatory cytokines, acute phase reactants and many proteases and protease inhibitors. Most of the proteins are made by microglia and astrocytes, but even neurons are producers. Many appear in association with Alzheimer disease lesions, indicating a state of chronic inflammation in Alzheimer disease brain. Such a state can apparently exist without stimulation by peripheral inflammatory mediators or the peripheral immune system. A strong inflammatory response may be autotoxic to neurons, exacerbating the fundamental pathology in Alzheimer disease and perhaps other neurological disorders. Autotoxic processes may contribute to cellular death in chronic inflammatory diseases affecting other parts of the body, suggesting the general therapeutic value of anti-inflammatory agents. With respect to Alzheimer disease, multiple epidemiological studies indicate that patients taking anti-inflammatory drugs or suffering from conditions in which such drugs are routinely used, have a decreased risk of developing Alzheimer disease. In one very preliminary clinical trial, the anti-inflammatory drug indomethacin arrested progress of the disease. 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Fax: (1) (604) 822-7086.</p></note><affiliation>Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., V6T 1Z3, Canada</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Edith G.</forename><surname>McGeer</surname></persName><affiliation>Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., V6T 1Z3, Canada</affiliation></author><idno type="istex">BCFA039A181F764FF3A458485F6FCCBA6F7C917D</idno><idno type="DOI">10.1016/0165-0173(95)00011-9</idno><idno type="PII">0165-0173(95)00011-9</idno></analytic><monogr><title level="j">Brain Research Reviews</title><title level="j" type="abbrev">BRESR</title><idno type="pISSN">0165-0173</idno><idno type="PII">S0165-0173(00)X0002-1</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1996"></date><biblScope unit="volume">21</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="195">195</biblScope><biblScope unit="page" to="218">218</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1996</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Cultured brain cells are capable of generating many molecules associated with inflammatory and immune functions. They constitute the endogenous immune response system of brain. They include complement proteins and their regulators, inflammatory cytokines, acute phase reactants and many proteases and protease inhibitors. Most of the proteins are made by microglia and astrocytes, but even neurons are producers. Many appear in association with Alzheimer disease lesions, indicating a state of chronic inflammation in Alzheimer disease brain. Such a state can apparently exist without stimulation by peripheral inflammatory mediators or the peripheral immune system. A strong inflammatory response may be autotoxic to neurons, exacerbating the fundamental pathology in Alzheimer disease and perhaps other neurological disorders. Autotoxic processes may contribute to cellular death in chronic inflammatory diseases affecting other parts of the body, suggesting the general therapeutic value of anti-inflammatory agents. With respect to Alzheimer disease, multiple epidemiological studies indicate that patients taking anti-inflammatory drugs or suffering from conditions in which such drugs are routinely used, have a decreased risk of developing Alzheimer disease. In one very preliminary clinical trial, the anti-inflammatory drug indomethacin arrested progress of the disease. New agents directed against the inflammatory processes revealed in studies of Alzheimer disease lesions may have broad therapeutic applications.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Complement</term></item><item><term>Microglia</term></item><item><term>Astrocyte</term></item><item><term>Cytokine</term></item><item><term>Anti-inflammatory agent</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1996">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api-v5.istex.fr/document/BCFA039A181F764FF3A458485F6FCCBA6F7C917D/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="rev"><item-info><jid>BRESR</jid><aid>95000119</aid><ce:pii>0165-0173(95)00011-9</ce:pii><ce:doi>10.1016/0165-0173(95)00011-9</ce:doi><ce:copyright type="unknown" year="1996"></ce:copyright></item-info><head><ce:dochead><ce:textfn>Review article</ce:textfn></ce:dochead><ce:title>The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases</ce:title><ce:author-group><ce:author><ce:given-name>Patrick L.</ce:given-name><ce:surname>McGeer</ce:surname><ce:cross-ref refid="COR1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Edith G.</ce:given-name><ce:surname>McGeer</ce:surname></ce:author><ce:affiliation><ce:textfn>Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., V6T 1Z3, Canada</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Corresponding author. Fax: (1) (604) 822-7086.</ce:text></ce:correspondence></ce:author-group><ce:date-accepted day="28" month="9" year="1995"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Cultured brain cells are capable of generating many molecules associated with inflammatory and immune functions. They constitute the endogenous immune response system of brain. They include complement proteins and their regulators, inflammatory cytokines, acute phase reactants and many proteases and protease inhibitors. Most of the proteins are made by microglia and astrocytes, but even neurons are producers. Many appear in association with Alzheimer disease lesions, indicating a state of chronic inflammation in Alzheimer disease brain. Such a state can apparently exist without stimulation by peripheral inflammatory mediators or the peripheral immune system. A strong inflammatory response may be autotoxic to neurons, exacerbating the fundamental pathology in Alzheimer disease and perhaps other neurological disorders. Autotoxic processes may contribute to cellular death in chronic inflammatory diseases affecting other parts of the body, suggesting the general therapeutic value of anti-inflammatory agents. With respect to Alzheimer disease, multiple epidemiological studies indicate that patients taking anti-inflammatory drugs or suffering from conditions in which such drugs are routinely used, have a decreased risk of developing Alzheimer disease. In one very preliminary clinical trial, the anti-inflammatory drug indomethacin arrested progress of the disease. 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With respect to Alzheimer disease, multiple epidemiological studies indicate that patients taking anti-inflammatory drugs or suffering from conditions in which such drugs are routinely used, have a decreased risk of developing Alzheimer disease. In one very preliminary clinical trial, the anti-inflammatory drug indomethacin arrested progress of the disease. New agents directed against the inflammatory processes revealed in studies of Alzheimer disease lesions may have broad therapeutic applications.</abstract><note type="content">Section title: Review article</note><subject><genre>Keywords</genre><topic>Complement</topic><topic>Microglia</topic><topic>Astrocyte</topic><topic>Cytokine</topic><topic>Anti-inflammatory agent</topic></subject><relatedItem type="host"><titleInfo><title>Brain Research Reviews</title></titleInfo><titleInfo type="abbreviated"><title>BRESR</title></titleInfo><genre type="journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">199509</dateIssued></originInfo><identifier type="ISSN">0165-0173</identifier><identifier type="PII">S0165-0173(00)X0002-1</identifier><part><date>199509</date><detail type="volume"><number>21</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue pages"><start>117</start><end>218</end></extent><extent unit="pages"><start>195</start><end>218</end></extent></part></relatedItem><identifier type="istex">BCFA039A181F764FF3A458485F6FCCBA6F7C917D</identifier><identifier type="DOI">10.1016/0165-0173(95)00011-9</identifier><identifier type="PII">0165-0173(95)00011-9</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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