Mechanisms of cell death in Alzheimer disease--immunopathology.
Identifieur interne : 003855 ( Main/Exploration ); précédent : 003854; suivant : 003856Mechanisms of cell death in Alzheimer disease--immunopathology.
Auteurs : P L Mcgeer [Canada] ; E G McgeerSource :
- Journal of neural transmission. Supplementum [ 0303-6995 ] ; 1998.
English descriptors
- KwdEn :
- MESH :
- immunology : Alzheimer Disease, Brain, Parkinson Disease.
- pathology : Alzheimer Disease, Astrocytes, Brain, Microglia, Neurons, Parkinson Disease.
- Humans, Inflammation, Models, Immunological, Models, Neurological.
Abstract
Lesions in such chronic neurodegenerative disorders as Alzheimer disease, Parkinson disease, the parkinsonism dementia complex of Guam and amyotrophic lateral sclerosis have associated with them a variety of proteins known to be involved in inflammatory processes. This is particularly true of Alzheimer disease where inflammatory reactions are thought to be important contributors to the neuronal loss. They include complement proteins, complement inhibitors, acute phase reactants, inflammatory cytokines, proteases and protease inhibitors. Studies of cultured human astrocytes and microglia, obtained from postmortem brain, have established that nearly all of these proteins are produced by one or another of these cell types. Human neurons also produce many inflammatory proteins and their inhibitors, creating complex interactions. Accumulations of amyloid and extracellular tangles apparently act as irritants, causing the activation of complement, the initiation of reactive changes in microglia, and the release of potentially neurotoxic products. Such products include the membrane attack complex, oxygen free radicals and excess glutamate. Twenty epidemiological studies that have been published to data indicate that populations taking antiinflammatory drugs have a significantly reduced prevalence of Alzheimer disease or a slower mental decline. One small clinical trial with indomethacin showed arrest of the disease over a 6 month period. Therapeutic intervention in key inflammatory processes holds great promise for the amelioration of Alzheimer disease and possibly other neurodegenerative disorders.
PubMed: 9850924
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 001792
- to stream PubMed, to step Curation: 001792
- to stream PubMed, to step Checkpoint: 001792
- to stream Ncbi, to step Merge: 002674
- to stream Ncbi, to step Curation: 002674
- to stream Ncbi, to step Checkpoint: 002674
- to stream Main, to step Merge: 003E56
- to stream Main, to step Curation: 003855
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Mechanisms of cell death in Alzheimer disease--immunopathology.</title>
<author><name sortKey="Mcgeer, P L" sort="Mcgeer, P L" uniqKey="Mcgeer P" first="P L" last="Mcgeer">P L Mcgeer</name>
<affiliation wicri:level="1"><nlm:affiliation>Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, Canada.</nlm:affiliation>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver</wicri:regionArea>
<wicri:noRegion>Vancouver</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Mcgeer, E G" sort="Mcgeer, E G" uniqKey="Mcgeer E" first="E G" last="Mcgeer">E G Mcgeer</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="1998">1998</date>
<idno type="RBID">pubmed:9850924</idno>
<idno type="pmid">9850924</idno>
<idno type="wicri:Area/PubMed/Corpus">001792</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001792</idno>
<idno type="wicri:Area/PubMed/Curation">001792</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001792</idno>
<idno type="wicri:Area/PubMed/Checkpoint">001792</idno>
<idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001792</idno>
<idno type="wicri:Area/Ncbi/Merge">002674</idno>
<idno type="wicri:Area/Ncbi/Curation">002674</idno>
<idno type="wicri:Area/Ncbi/Checkpoint">002674</idno>
<idno type="wicri:doubleKey">0303-6995:1998:Mcgeer P:mechanisms:of:cell</idno>
<idno type="wicri:Area/Main/Merge">003E56</idno>
<idno type="wicri:Area/Main/Curation">003855</idno>
<idno type="wicri:Area/Main/Exploration">003855</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">Mechanisms of cell death in Alzheimer disease--immunopathology.</title>
<author><name sortKey="Mcgeer, P L" sort="Mcgeer, P L" uniqKey="Mcgeer P" first="P L" last="Mcgeer">P L Mcgeer</name>
<affiliation wicri:level="1"><nlm:affiliation>Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, Canada.</nlm:affiliation>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver</wicri:regionArea>
<wicri:noRegion>Vancouver</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Mcgeer, E G" sort="Mcgeer, E G" uniqKey="Mcgeer E" first="E G" last="Mcgeer">E G Mcgeer</name>
</author>
</analytic>
<series><title level="j">Journal of neural transmission. Supplementum</title>
<idno type="ISSN">0303-6995</idno>
<imprint><date when="1998" type="published">1998</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alzheimer Disease (immunology)</term>
<term>Alzheimer Disease (pathology)</term>
<term>Astrocytes (pathology)</term>
<term>Brain (immunology)</term>
<term>Brain (pathology)</term>
<term>Humans</term>
<term>Inflammation</term>
<term>Microglia (pathology)</term>
<term>Models, Immunological</term>
<term>Models, Neurological</term>
<term>Neurons (pathology)</term>
<term>Parkinson Disease (immunology)</term>
<term>Parkinson Disease (pathology)</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Alzheimer Disease</term>
<term>Brain</term>
<term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Alzheimer Disease</term>
<term>Astrocytes</term>
<term>Brain</term>
<term>Microglia</term>
<term>Neurons</term>
<term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Humans</term>
<term>Inflammation</term>
<term>Models, Immunological</term>
<term>Models, Neurological</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Lesions in such chronic neurodegenerative disorders as Alzheimer disease, Parkinson disease, the parkinsonism dementia complex of Guam and amyotrophic lateral sclerosis have associated with them a variety of proteins known to be involved in inflammatory processes. This is particularly true of Alzheimer disease where inflammatory reactions are thought to be important contributors to the neuronal loss. They include complement proteins, complement inhibitors, acute phase reactants, inflammatory cytokines, proteases and protease inhibitors. Studies of cultured human astrocytes and microglia, obtained from postmortem brain, have established that nearly all of these proteins are produced by one or another of these cell types. Human neurons also produce many inflammatory proteins and their inhibitors, creating complex interactions. Accumulations of amyloid and extracellular tangles apparently act as irritants, causing the activation of complement, the initiation of reactive changes in microglia, and the release of potentially neurotoxic products. Such products include the membrane attack complex, oxygen free radicals and excess glutamate. Twenty epidemiological studies that have been published to data indicate that populations taking antiinflammatory drugs have a significantly reduced prevalence of Alzheimer disease or a slower mental decline. One small clinical trial with indomethacin showed arrest of the disease over a 6 month period. Therapeutic intervention in key inflammatory processes holds great promise for the amelioration of Alzheimer disease and possibly other neurodegenerative disorders.</div>
</front>
</TEI>
<affiliations><list><country><li>Canada</li>
</country>
</list>
<tree><noCountry><name sortKey="Mcgeer, E G" sort="Mcgeer, E G" uniqKey="Mcgeer E" first="E G" last="Mcgeer">E G Mcgeer</name>
</noCountry>
<country name="Canada"><noRegion><name sortKey="Mcgeer, P L" sort="Mcgeer, P L" uniqKey="Mcgeer P" first="P L" last="Mcgeer">P L Mcgeer</name>
</noRegion>
</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 003855 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 003855 | 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= pubmed:9850924 |texte= Mechanisms of cell death in Alzheimer disease--immunopathology. }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:9850924" \ | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \ | NlmPubMed2Wicri -a ParkinsonCanadaV1
This area was generated with Dilib version V0.6.29. |