Inflammation and Alzheimer's disease pathogenesis

Appreciation of the role that inflammatory mediators play in Alzheimer's disease (AD) pathogenesis continues to be hampered by two related misconceptions. The first is that to be pathogenically significant a neurodegenerative mechanism must be primary. The second is that inflammation merely occ...

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Published in	Neurobiology of aging Vol. 17; no. 5; pp. 681 - 686
Main Authors	Rogers, Joseph, Webster, Scott, Lue, Lih-Fen, Brachova, Libuse, Harold Civin, W., Emmerling, Mark, Shivers, Brenda, Walker, Douglas, McGeer, Patrick
Format	Journal Article
Language	English
Published	United States Elsevier Inc 01.09.1996
Subjects	Alzheimer Disease - drug therapy Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Anti-Inflammatory Agents, Non-Steroidal - therapeutic use Brain Chemistry - drug effects Complement Cytokines Dementia Humans Inflammation Inflammation - metabolism Inflammation - pathology Inflammation Mediators - physiology Neurodegeneration Inflammation Complement Cytokines Neurodegeneration Alzheimer's disease Dementia
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Abstract	Appreciation of the role that inflammatory mediators play in Alzheimer's disease (AD) pathogenesis continues to be hampered by two related misconceptions. The first is that to be pathogenically significant a neurodegenerative mechanism must be primary. The second is that inflammation merely occurs to clear the detritis of already existant pathology. The present review addresses these issues by showing that 1) inflammatory molecules and mechanisms are uniquely present or significantly elevated in the AD brain, 2) inflammation may be a necessary component of AD pathogenssis, 3) inflammation may be sufficient to cause AD neurodegeneration, and 4) retrospective and direct clinical trials suggest a therapeutic benefit of conventional antiinflammatory medications in slowing the progress or even delaying the onset of AD.
AbstractList	Appreciation of the role that inflammatory mediators play in Alzheimer's disease (AD) pathogenesis continues to be hampered by two related misconceptions. The first is that to be pathogenically significant a neurodegenerative mechanism must be primary. The second is that inflammation merely occurs to clear the detritis of already existant pathology. The present review addresses these issues by showing that 1) inflammatory molecules and mechanisms are uniquely present or significantly elevated in the AD brain, 2) inflammation may be a necessary component of AD pathogenssis, 3) inflammation may be sufficient to cause AD neurodegeneration, and 4) retrospective and direct clinical trials suggest a therapeutic benefit of conventional antiinflammatory medications in slowing the progress or even delaying the onset of AD. Appreciation of the role that inflammatory mediators play in Alzheimer's disease (AD) pathogenesis continues to be hampered by two related misconceptions. The first is that to be pathogenically significant a neurodegenerative mechanism must be primary. The second is that inflammation merely occurs to clear the detritis of already existant pathology. The present review addresses these issues by showing that 1) inflammatory molecules and mechanisms are uniquely present or significantly elevated in the AD brain, 2) inflammation may be a necessary component of AD pathogenesis, 3) inflammation may be sufficient to cause AD neurodegeneration, and 4) retrospective and direct clinical trials suggest a therapeutic benefit of conventional antiinflammatory medications in slowing the progress or even delaying the onset of AD. Appreciation of the role that inflammatory mediators play in Alzheimer's disease (AD) pathogenesis continues to be hampered by two related misconceptions. The first is that to be pathogenically significant a neurodegenerative mechanism must be primary. The second is that inflammation merely occurs to clear the detritis of already existent pathology. The present review addresses these issues by showing that 1) inflammatory molecules and mechanisms are uniquely present or significantly elevated in the AD brain, 2) inflammation may be a necessary component of AD pathogenesis, 3) inflammation may be sufficient to cause AD neurodegeneration, and 4) retrospective and direct clinical trials suggest a therapeutic benefit of conventional antiinflammatory medications in slowing the progress or even delaying the onset of AD.
Author	Webster, Scott McGeer, Patrick Shivers, Brenda Lue, Lih-Fen Harold Civin, W. Brachova, Libuse Rogers, Joseph Walker, Douglas Emmerling, Mark
Author_xml	– sequence: 1 givenname: Joseph surname: Rogers fullname: Rogers, Joseph organization: Sun Health Research Institute, 10515 West Santa Fe Drive, P.O. Box 1278, Sun City, AZ 85372, USA – sequence: 2 givenname: Scott surname: Webster fullname: Webster, Scott organization: Sun Health Research Institute, 10515 West Santa Fe Drive, P.O. Box 1278, Sun City, AZ 85372, USA – sequence: 3 givenname: Lih-Fen surname: Lue fullname: Lue, Lih-Fen organization: Sun Health Research Institute, 10515 West Santa Fe Drive, P.O. Box 1278, Sun City, AZ 85372, USA – sequence: 4 givenname: Libuse surname: Brachova fullname: Brachova, Libuse organization: Sun Health Research Institute, 10515 West Santa Fe Drive, P.O. Box 1278, Sun City, AZ 85372, USA – sequence: 5 givenname: W. surname: Harold Civin fullname: Harold Civin, W. organization: Sun Health Research Institute, 10515 West Santa Fe Drive, P.O. Box 1278, Sun City, AZ 85372, USA – sequence: 6 givenname: Mark surname: Emmerling fullname: Emmerling, Mark organization: Sun Health Research Institute, 10515 West Santa Fe Drive, P.O. Box 1278, Sun City, AZ 85372, USA – sequence: 7 givenname: Brenda surname: Shivers fullname: Shivers, Brenda organization: Sun Health Research Institute, 10515 West Santa Fe Drive, P.O. Box 1278, Sun City, AZ 85372, USA – sequence: 8 givenname: Douglas surname: Walker fullname: Walker, Douglas organization: Sun Health Research Institute, 10515 West Santa Fe Drive, P.O. Box 1278, Sun City, AZ 85372, USA – sequence: 9 givenname: Patrick surname: McGeer fullname: McGeer, Patrick organization: Sun Health Research Institute, 10515 West Santa Fe Drive, P.O. Box 1278, Sun City, AZ 85372, USA
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/8892340$$D View this record in MEDLINE/PubMed
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Snippet	Appreciation of the role that inflammatory mediators play in Alzheimer's disease (AD) pathogenesis continues to be hampered by two related misconceptions. The...
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SubjectTerms	Alzheimer Disease - drug therapy Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Anti-Inflammatory Agents, Non-Steroidal - therapeutic use Brain Chemistry - drug effects Complement Cytokines Dementia Humans Inflammation Inflammation - metabolism Inflammation - pathology Inflammation Mediators - physiology Neurodegeneration
Title	Inflammation and Alzheimer's disease pathogenesis
URI	https://dx.doi.org/10.1016/0197-4580(96)00115-7 https://www.ncbi.nlm.nih.gov/pubmed/8892340 https://search.proquest.com/docview/15961259 https://search.proquest.com/docview/78481158
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