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...
Gespeichert in:
Veröffentlicht in: | Neurobiology of aging 1996-09, Vol.17 (5), p.681-686 |
---|---|
Hauptverfasser: | , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 686 |
---|---|
container_issue | 5 |
container_start_page | 681 |
container_title | Neurobiology of aging |
container_volume | 17 |
creator | Rogers, Joseph Webster, Scott Lue, Lih-Fen Brachova, Libuse Harold Civin, W. Emmerling, Mark Shivers, Brenda Walker, Douglas McGeer, Patrick |
description | 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. |
doi_str_mv | 10.1016/0197-4580(96)00115-7 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_78481158</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>0197458096001157</els_id><sourcerecordid>78481158</sourcerecordid><originalsourceid>FETCH-LOGICAL-c454t-c21f4258362ccfaa4f9aa4df53779883fc22f3648713af8214d3776dbdaeffeb3</originalsourceid><addsrcrecordid>eNqFkE1LAzEQhoMotVb_gcKe_DisJtlkk1yEUvwoFLzoOaTJxEb2o262gv56s7T0qJcZhvd9Z5gHoXOCbwkm5R0mSuSMS3ytyhuMCeG5OEBjwrnMCVPiEI33lmN0EuMHxlgwUY7QSEpFC4bHiMwbX5m6Nn1om8w0LptWPysINXRXMXMhgomQrU2_at-hgRjiKTrypopwtusT9Pb48Dp7zhcvT_PZdJFbxlmfW0o8o1wWJbXWG8O8SsV5XgihpCy8pdQXJZOCFMZLSphLSumWzoD3sCwm6HK7d921nxuIva5DtFBVpoF2E7WQTKaf5b9GwlVJKFfJyLZG27UxduD1ugu16b41wXpAqgdeeuClVRoGpFqk2MVu_2ZZg9uHdgyTfr_VIdH4CtDpaAM0FlzowPbateHvA7_LHYS7</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>15961259</pqid></control><display><type>article</type><title>Inflammation and Alzheimer's disease pathogenesis</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Rogers, Joseph ; Webster, Scott ; Lue, Lih-Fen ; Brachova, Libuse ; Harold Civin, W. ; Emmerling, Mark ; Shivers, Brenda ; Walker, Douglas ; McGeer, Patrick</creator><creatorcontrib>Rogers, Joseph ; Webster, Scott ; Lue, Lih-Fen ; Brachova, Libuse ; Harold Civin, W. ; Emmerling, Mark ; Shivers, Brenda ; Walker, Douglas ; McGeer, Patrick</creatorcontrib><description>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.</description><identifier>ISSN: 0197-4580</identifier><identifier>EISSN: 1558-1497</identifier><identifier>DOI: 10.1016/0197-4580(96)00115-7</identifier><identifier>PMID: 8892340</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>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</subject><ispartof>Neurobiology of aging, 1996-09, Vol.17 (5), p.681-686</ispartof><rights>1996</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c454t-c21f4258362ccfaa4f9aa4df53779883fc22f3648713af8214d3776dbdaeffeb3</citedby><cites>FETCH-LOGICAL-c454t-c21f4258362ccfaa4f9aa4df53779883fc22f3648713af8214d3776dbdaeffeb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/0197458096001157$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8892340$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rogers, Joseph</creatorcontrib><creatorcontrib>Webster, Scott</creatorcontrib><creatorcontrib>Lue, Lih-Fen</creatorcontrib><creatorcontrib>Brachova, Libuse</creatorcontrib><creatorcontrib>Harold Civin, W.</creatorcontrib><creatorcontrib>Emmerling, Mark</creatorcontrib><creatorcontrib>Shivers, Brenda</creatorcontrib><creatorcontrib>Walker, Douglas</creatorcontrib><creatorcontrib>McGeer, Patrick</creatorcontrib><title>Inflammation and Alzheimer's disease pathogenesis</title><title>Neurobiology of aging</title><addtitle>Neurobiol Aging</addtitle><description>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.</description><subject>Alzheimer Disease - drug therapy</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer's disease</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - therapeutic use</subject><subject>Brain Chemistry - drug effects</subject><subject>Complement</subject><subject>Cytokines</subject><subject>Dementia</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Inflammation Mediators - physiology</subject><subject>Neurodegeneration</subject><issn>0197-4580</issn><issn>1558-1497</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1LAzEQhoMotVb_gcKe_DisJtlkk1yEUvwoFLzoOaTJxEb2o262gv56s7T0qJcZhvd9Z5gHoXOCbwkm5R0mSuSMS3ytyhuMCeG5OEBjwrnMCVPiEI33lmN0EuMHxlgwUY7QSEpFC4bHiMwbX5m6Nn1om8w0LptWPysINXRXMXMhgomQrU2_at-hgRjiKTrypopwtusT9Pb48Dp7zhcvT_PZdJFbxlmfW0o8o1wWJbXWG8O8SsV5XgihpCy8pdQXJZOCFMZLSphLSumWzoD3sCwm6HK7d921nxuIva5DtFBVpoF2E7WQTKaf5b9GwlVJKFfJyLZG27UxduD1ugu16b41wXpAqgdeeuClVRoGpFqk2MVu_2ZZg9uHdgyTfr_VIdH4CtDpaAM0FlzowPbateHvA7_LHYS7</recordid><startdate>19960901</startdate><enddate>19960901</enddate><creator>Rogers, Joseph</creator><creator>Webster, Scott</creator><creator>Lue, Lih-Fen</creator><creator>Brachova, Libuse</creator><creator>Harold Civin, W.</creator><creator>Emmerling, Mark</creator><creator>Shivers, Brenda</creator><creator>Walker, Douglas</creator><creator>McGeer, Patrick</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>19960901</creationdate><title>Inflammation and Alzheimer's disease pathogenesis</title><author>Rogers, Joseph ; Webster, Scott ; Lue, Lih-Fen ; Brachova, Libuse ; Harold Civin, W. ; Emmerling, Mark ; Shivers, Brenda ; Walker, Douglas ; McGeer, Patrick</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c454t-c21f4258362ccfaa4f9aa4df53779883fc22f3648713af8214d3776dbdaeffeb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Alzheimer Disease - drug therapy</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer Disease - pathology</topic><topic>Alzheimer's disease</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - therapeutic use</topic><topic>Brain Chemistry - drug effects</topic><topic>Complement</topic><topic>Cytokines</topic><topic>Dementia</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - pathology</topic><topic>Inflammation Mediators - physiology</topic><topic>Neurodegeneration</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rogers, Joseph</creatorcontrib><creatorcontrib>Webster, Scott</creatorcontrib><creatorcontrib>Lue, Lih-Fen</creatorcontrib><creatorcontrib>Brachova, Libuse</creatorcontrib><creatorcontrib>Harold Civin, W.</creatorcontrib><creatorcontrib>Emmerling, Mark</creatorcontrib><creatorcontrib>Shivers, Brenda</creatorcontrib><creatorcontrib>Walker, Douglas</creatorcontrib><creatorcontrib>McGeer, Patrick</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neurobiology of aging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rogers, Joseph</au><au>Webster, Scott</au><au>Lue, Lih-Fen</au><au>Brachova, Libuse</au><au>Harold Civin, W.</au><au>Emmerling, Mark</au><au>Shivers, Brenda</au><au>Walker, Douglas</au><au>McGeer, Patrick</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inflammation and Alzheimer's disease pathogenesis</atitle><jtitle>Neurobiology of aging</jtitle><addtitle>Neurobiol Aging</addtitle><date>1996-09-01</date><risdate>1996</risdate><volume>17</volume><issue>5</issue><spage>681</spage><epage>686</epage><pages>681-686</pages><issn>0197-4580</issn><eissn>1558-1497</eissn><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.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>8892340</pmid><doi>10.1016/0197-4580(96)00115-7</doi><tpages>6</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0197-4580 |
ispartof | Neurobiology of aging, 1996-09, Vol.17 (5), p.681-686 |
issn | 0197-4580 1558-1497 |
language | eng |
recordid | cdi_proquest_miscellaneous_78481158 |
source | MEDLINE; Elsevier ScienceDirect Journals |
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 |
title | Inflammation and Alzheimer's disease pathogenesis |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-01T23%3A36%3A35IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Inflammation%20and%20Alzheimer's%20disease%20pathogenesis&rft.jtitle=Neurobiology%20of%20aging&rft.au=Rogers,%20Joseph&rft.date=1996-09-01&rft.volume=17&rft.issue=5&rft.spage=681&rft.epage=686&rft.pages=681-686&rft.issn=0197-4580&rft.eissn=1558-1497&rft_id=info:doi/10.1016/0197-4580(96)00115-7&rft_dat=%3Cproquest_cross%3E78481158%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=15961259&rft_id=info:pmid/8892340&rft_els_id=0197458096001157&rfr_iscdi=true |