The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases
Identifieur interne : 003D27 ( Main/Exploration ); précédent : 003D26; suivant : 003D28The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases
Auteurs : Patrick L. Mcgeer [Canada] ; Edith G. Mcgeer [Canada]Source :
- 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
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream Istex, to step Corpus: 002967
- to stream Istex, to step Curation: 002967
- to stream Istex, to step Checkpoint: 001737
- to stream Main, to step Merge: 004417
- to stream Main, to step Curation: 003D27
Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases</title>
<author><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L." last="Mcgeer">Patrick L. Mcgeer</name>
</author>
<author><name sortKey="Mcgeer, Edith G" sort="Mcgeer, Edith G" uniqKey="Mcgeer E" first="Edith G." last="Mcgeer">Edith G. Mcgeer</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">ISTEX</idno>
<idno type="RBID">ISTEX:BCFA039A181F764FF3A458485F6FCCBA6F7C917D</idno>
<date when="1996" year="1996">1996</date>
<idno type="doi">10.1016/0165-0173(95)00011-9</idno>
<idno type="url">https://api-v5.istex.fr/document/BCFA039A181F764FF3A458485F6FCCBA6F7C917D/fulltext/pdf</idno>
<idno type="wicri:Area/Istex/Corpus">002967</idno>
<idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">002967</idno>
<idno type="wicri:Area/Istex/Curation">002967</idno>
<idno type="wicri:Area/Istex/Checkpoint">001737</idno>
<idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">001737</idno>
<idno type="wicri:doubleKey">0165-0173:1996:Mcgeer P:the:inflammatory:response</idno>
<idno type="wicri:Area/Main/Merge">004417</idno>
<idno type="wicri:Area/Main/Curation">003D27</idno>
<idno type="wicri:Area/Main/Exploration">003D27</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title level="a">The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases</title>
<author><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L." last="Mcgeer">Patrick L. Mcgeer</name>
<affiliation wicri:level="1"><country xml:lang="fr">Canada</country>
<wicri:regionArea>Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., V6T 1Z3</wicri:regionArea>
<wicri:noRegion>V6T 1Z3</wicri:noRegion>
</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 wicri:level="1"><country xml:lang="fr">Canada</country>
<wicri:regionArea>Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, B.C., V6T 1Z3</wicri:regionArea>
<wicri:noRegion>V6T 1Z3</wicri:noRegion>
</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>
<affiliations><list><country><li>Canada</li>
</country>
</list>
<tree><country name="Canada"><noRegion><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L." last="Mcgeer">Patrick L. Mcgeer</name>
</noRegion>
<name sortKey="Mcgeer, Edith G" sort="Mcgeer, Edith G" uniqKey="Mcgeer E" first="Edith G." last="Mcgeer">Edith G. Mcgeer</name>
</country>
</tree>
</affiliations>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Canada/explor/ParkinsonCanadaV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 003D27 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 003D27 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Canada |area= ParkinsonCanadaV1 |flux= Main |étape= Exploration |type= RBID |clé= ISTEX:BCFA039A181F764FF3A458485F6FCCBA6F7C917D |texte= The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases }}
![]() | This area was generated with Dilib version V0.6.29. | ![]() |