Innate immunity, local inflammation, and degenerative disease.
Identifieur interne : 002F72 ( Main/Exploration ); précédent : 002F71; suivant : 002F73Innate immunity, local inflammation, and degenerative disease.
Auteurs : Patrick L. Mcgeer [Canada] ; Edith G. McgeerSource :
- Science of aging knowledge environment : SAGE KE [ 1539-6150 ] ; 2002.
English descriptors
- KwdEn :
- Alzheimer Disease (immunology), Alzheimer Disease (metabolism), Alzheimer Disease (pathology), Alzheimer Disease (prevention & control), Animals, Anti-Inflammatory Agents, Non-Steroidal (therapeutic use), Humans, Immunity, Innate (immunology), Inflammation (immunology), Inflammation (metabolism), Inflammation (pathology), Inflammation Mediators (immunology), Inflammation Mediators (metabolism), Parkinson Disease (immunology), Parkinson Disease (metabolism), Parkinson Disease (prevention & control).
- MESH :
- chemical , immunology : Inflammation Mediators.
- chemical , metabolism : Inflammation Mediators.
- chemical , therapeutic use : Anti-Inflammatory Agents, Non-Steroidal.
- immunology : Alzheimer Disease, Immunity, Innate, Inflammation, Parkinson Disease.
- metabolism : Alzheimer Disease, Inflammation, Parkinson Disease.
- pathology : Alzheimer Disease, Inflammation.
- prevention & control : Alzheimer Disease, Parkinson Disease.
- Animals, Humans.
Abstract
The brain lesions associated with Alzheimer's disease (AD), which are referred to as neurofibrillary tangles and senile plaques, are characterized by the presence of a broad spectrum of inflammatory mediators. Surprisingly, these mediators, which include complement proteins, inflammatory cytokines, prostaglandins, and acute phase reactants such as C-reactive protein and amyloid P, are produced by resident brain cells, including neurons. Although secondary to the fundamental pathology caused by the presence of tangles and plaques, there is strong evidence that inflammation exacerbates the neuronal loss. In particular, AD lesions show evidence of self-attack by the complement system--a part of the immune system that normally functions to rid the body of invading pathogens. However, the lesions are devoid of significant T cell infiltration, a hallmark of an inflammatory immune response, and antibodies. We define this phenomenon as autotoxicity to distinguish it from classical autoimmunity, in which the body raises antibodies to normal endogenous macromolecules. Locally produced inflammatory mediators have also been identified in atherosclerotic plaques, along with evidence of complement self-attack. As was previously shown for heart attacks, epidemiological evidence indicates that extended use of nonsteroidal anti-inflammatory drugs (NSAIDs) results in a reduced risk of AD. NSAIDs inhibit the production of prostaglandin inflammatory mediators, but powerful new therapeutic agents might be developed by targeting more critical inflammatory mechanisms, especially the complement system.
DOI: 10.1126/sageke.2002.29.re3
PubMed: 14602998
Affiliations:
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Mcgeer</name><affiliation wicri:level="1"><nlm:affiliation>Kinsmen Laboratory of Neurological Research at the University of British Columbia, Vancouver, BC, V6T 1Z3, Canada. mcgeerpl@interchange.ubc.ca</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Kinsmen Laboratory of Neurological Research at the University of British Columbia, Vancouver, BC, 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></author></analytic><series><title level="j">Science of aging knowledge environment : SAGE KE</title><idno type="eISSN">1539-6150</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alzheimer Disease (immunology)</term><term>Alzheimer Disease (metabolism)</term><term>Alzheimer Disease (pathology)</term><term>Alzheimer Disease (prevention & control)</term><term>Animals</term><term>Anti-Inflammatory Agents, Non-Steroidal (therapeutic use)</term><term>Humans</term><term>Immunity, Innate (immunology)</term><term>Inflammation (immunology)</term><term>Inflammation (metabolism)</term><term>Inflammation (pathology)</term><term>Inflammation Mediators (immunology)</term><term>Inflammation Mediators (metabolism)</term><term>Parkinson Disease (immunology)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (prevention & control)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Inflammation Mediators</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Inflammation Mediators</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Anti-Inflammatory Agents, Non-Steroidal</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Alzheimer Disease</term><term>Immunity, Innate</term><term>Inflammation</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Alzheimer Disease</term><term>Inflammation</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Alzheimer Disease</term><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Alzheimer Disease</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The brain lesions associated with Alzheimer's disease (AD), which are referred to as neurofibrillary tangles and senile plaques, are characterized by the presence of a broad spectrum of inflammatory mediators. Surprisingly, these mediators, which include complement proteins, inflammatory cytokines, prostaglandins, and acute phase reactants such as C-reactive protein and amyloid P, are produced by resident brain cells, including neurons. Although secondary to the fundamental pathology caused by the presence of tangles and plaques, there is strong evidence that inflammation exacerbates the neuronal loss. In particular, AD lesions show evidence of self-attack by the complement system--a part of the immune system that normally functions to rid the body of invading pathogens. However, the lesions are devoid of significant T cell infiltration, a hallmark of an inflammatory immune response, and antibodies. We define this phenomenon as autotoxicity to distinguish it from classical autoimmunity, in which the body raises antibodies to normal endogenous macromolecules. Locally produced inflammatory mediators have also been identified in atherosclerotic plaques, along with evidence of complement self-attack. As was previously shown for heart attacks, epidemiological evidence indicates that extended use of nonsteroidal anti-inflammatory drugs (NSAIDs) results in a reduced risk of AD. NSAIDs inhibit the production of prostaglandin inflammatory mediators, but powerful new therapeutic agents might be developed by targeting more critical inflammatory mechanisms, especially the complement system.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Mcgeer, Edith G" sort="Mcgeer, Edith G" uniqKey="Mcgeer E" first="Edith G" last="Mcgeer">Edith G. Mcgeer</name></noCountry><country name="Canada"><noRegion><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L" last="Mcgeer">Patrick L. 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