Inflammation as a central mechanism in Alzheimer's disease
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized by cognitive decline and the presence of two core pathologies, amyloid β plaques and neurofibrillary tangles. Over the last decade, the presence of a sustained immune response in the brain has emerged as...
Gespeichert in:
Veröffentlicht in: | Alzheimer's & dementia : translational research & clinical interventions 2018, Vol.4 (1), p.575-590 |
---|---|
Hauptverfasser: | , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 590 |
---|---|
container_issue | 1 |
container_start_page | 575 |
container_title | Alzheimer's & dementia : translational research & clinical interventions |
container_volume | 4 |
creator | Kinney, Jefferson W. Bemiller, Shane M. Murtishaw, Andrew S. Leisgang, Amanda M. Salazar, Arnold M. Lamb, Bruce T. |
description | Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized by cognitive decline and the presence of two core pathologies, amyloid β plaques and neurofibrillary tangles. Over the last decade, the presence of a sustained immune response in the brain has emerged as a third core pathology in AD. The sustained activation of the brain's resident macrophages (microglia) and other immune cells has been demonstrated to exacerbate both amyloid and tau pathology and may serve as a link in the pathogenesis of the disorder. In the following review, we provide an overview of inflammation in AD and a detailed coverage of a number of microglia-related signaling mechanisms that have been implicated in AD. Additional information on microglia signaling and a number of cytokines in AD are also reviewed. We also review the potential connection of risk factors for AD and how they may be related to inflammatory mechanisms. |
doi_str_mv | 10.1016/j.trci.2018.06.014 |
format | Article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6214864</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S2352873718300490</els_id><sourcerecordid>2131244734</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5724-60cbbd9d0091b94472021a99e94ff4f5d2e036c47c0e70d8c0a9cecff4752be13</originalsourceid><addsrcrecordid>eNqNkE1LxDAQhoMoKrp_wIP0ppetkzRNWhFhXfxYWRBEzyFNp26WfmjSVfTX29JV9CJeJkPmnXdeHkIOKIQUqDhZhq0zNmRAkxBECJRvkF0WxWycyEhu_uh3yMj7JQDQmCVpFG-TnQg4CCrlLjmd1UWpq0q3tqkD7QMdGKxbp8ugQrPQtfVVYOtgUn4s0FbojnyQW4_a4z7ZKnTpcbR-98jj1eXD9GY8v7ueTSfzsYkl42MBJsvyNAdIaZZyLhkwqtMUU14UvIhzhhAJw6UBlJAnBnRq0HQzGbMMabRHzgff51VWYb6Op56drbR7V4226vektgv11LwqwShPBO8MjtcGrnlZoW9VZb3BstQ1NiuvGI0o64JFvZQNUuMa7x0W32coqJ67Wqqeu-q5KxCq494tHf4M-L3yRbkTXAyCN1vi-z8s1cP9lN12ZdZ_ghiunA0m2LF-teiUNxZrg7l1aFqVN_avkJ9yEKhH</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2131244734</pqid></control><display><type>article</type><title>Inflammation as a central mechanism in Alzheimer's disease</title><source>Wiley Online Library Open Access</source><source>DOAJ Directory of Open Access Journals</source><source>Wiley Online Library Journals Frontfile Complete</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Kinney, Jefferson W. ; Bemiller, Shane M. ; Murtishaw, Andrew S. ; Leisgang, Amanda M. ; Salazar, Arnold M. ; Lamb, Bruce T.</creator><creatorcontrib>Kinney, Jefferson W. ; Bemiller, Shane M. ; Murtishaw, Andrew S. ; Leisgang, Amanda M. ; Salazar, Arnold M. ; Lamb, Bruce T.</creatorcontrib><description>Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized by cognitive decline and the presence of two core pathologies, amyloid β plaques and neurofibrillary tangles. Over the last decade, the presence of a sustained immune response in the brain has emerged as a third core pathology in AD. The sustained activation of the brain's resident macrophages (microglia) and other immune cells has been demonstrated to exacerbate both amyloid and tau pathology and may serve as a link in the pathogenesis of the disorder. In the following review, we provide an overview of inflammation in AD and a detailed coverage of a number of microglia-related signaling mechanisms that have been implicated in AD. Additional information on microglia signaling and a number of cytokines in AD are also reviewed. We also review the potential connection of risk factors for AD and how they may be related to inflammatory mechanisms.</description><identifier>ISSN: 2352-8737</identifier><identifier>EISSN: 2352-8737</identifier><identifier>DOI: 10.1016/j.trci.2018.06.014</identifier><identifier>PMID: 30406177</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Alzheimer's disease ; Cytokines ; Inflammation ; Microglia ; Microglia receptors ; Special Issue from the Centers of Biomedical Research Excellence (COBRE) and Center for Neurodegeneration and Translational Neuroscience (CNTN)</subject><ispartof>Alzheimer's & dementia : translational research & clinical interventions, 2018, Vol.4 (1), p.575-590</ispartof><rights>2018</rights><rights>2018 The Authors. Published by Elsevier Inc. on behalf of the Alzheimer's Association.</rights><rights>2018 Published by Elsevier Inc. on behalf of the Alzheimer's Association. 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5724-60cbbd9d0091b94472021a99e94ff4f5d2e036c47c0e70d8c0a9cecff4752be13</citedby><cites>FETCH-LOGICAL-c5724-60cbbd9d0091b94472021a99e94ff4f5d2e036c47c0e70d8c0a9cecff4752be13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6214864/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6214864/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,4010,11541,27900,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30406177$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kinney, Jefferson W.</creatorcontrib><creatorcontrib>Bemiller, Shane M.</creatorcontrib><creatorcontrib>Murtishaw, Andrew S.</creatorcontrib><creatorcontrib>Leisgang, Amanda M.</creatorcontrib><creatorcontrib>Salazar, Arnold M.</creatorcontrib><creatorcontrib>Lamb, Bruce T.</creatorcontrib><title>Inflammation as a central mechanism in Alzheimer's disease</title><title>Alzheimer's & dementia : translational research & clinical interventions</title><addtitle>Alzheimers Dement (N Y)</addtitle><description>Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized by cognitive decline and the presence of two core pathologies, amyloid β plaques and neurofibrillary tangles. Over the last decade, the presence of a sustained immune response in the brain has emerged as a third core pathology in AD. The sustained activation of the brain's resident macrophages (microglia) and other immune cells has been demonstrated to exacerbate both amyloid and tau pathology and may serve as a link in the pathogenesis of the disorder. In the following review, we provide an overview of inflammation in AD and a detailed coverage of a number of microglia-related signaling mechanisms that have been implicated in AD. Additional information on microglia signaling and a number of cytokines in AD are also reviewed. We also review the potential connection of risk factors for AD and how they may be related to inflammatory mechanisms.</description><subject>Alzheimer's disease</subject><subject>Cytokines</subject><subject>Inflammation</subject><subject>Microglia</subject><subject>Microglia receptors</subject><subject>Special Issue from the Centers of Biomedical Research Excellence (COBRE) and Center for Neurodegeneration and Translational Neuroscience (CNTN)</subject><issn>2352-8737</issn><issn>2352-8737</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><recordid>eNqNkE1LxDAQhoMoKrp_wIP0ppetkzRNWhFhXfxYWRBEzyFNp26WfmjSVfTX29JV9CJeJkPmnXdeHkIOKIQUqDhZhq0zNmRAkxBECJRvkF0WxWycyEhu_uh3yMj7JQDQmCVpFG-TnQg4CCrlLjmd1UWpq0q3tqkD7QMdGKxbp8ugQrPQtfVVYOtgUn4s0FbojnyQW4_a4z7ZKnTpcbR-98jj1eXD9GY8v7ueTSfzsYkl42MBJsvyNAdIaZZyLhkwqtMUU14UvIhzhhAJw6UBlJAnBnRq0HQzGbMMabRHzgff51VWYb6Op56drbR7V4226vektgv11LwqwShPBO8MjtcGrnlZoW9VZb3BstQ1NiuvGI0o64JFvZQNUuMa7x0W32coqJ67Wqqeu-q5KxCq494tHf4M-L3yRbkTXAyCN1vi-z8s1cP9lN12ZdZ_ghiunA0m2LF-teiUNxZrg7l1aFqVN_avkJ9yEKhH</recordid><startdate>2018</startdate><enddate>2018</enddate><creator>Kinney, Jefferson W.</creator><creator>Bemiller, Shane M.</creator><creator>Murtishaw, Andrew S.</creator><creator>Leisgang, Amanda M.</creator><creator>Salazar, Arnold M.</creator><creator>Lamb, Bruce T.</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</scope><scope>24P</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>2018</creationdate><title>Inflammation as a central mechanism in Alzheimer's disease</title><author>Kinney, Jefferson W. ; Bemiller, Shane M. ; Murtishaw, Andrew S. ; Leisgang, Amanda M. ; Salazar, Arnold M. ; Lamb, Bruce T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5724-60cbbd9d0091b94472021a99e94ff4f5d2e036c47c0e70d8c0a9cecff4752be13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Alzheimer's disease</topic><topic>Cytokines</topic><topic>Inflammation</topic><topic>Microglia</topic><topic>Microglia receptors</topic><topic>Special Issue from the Centers of Biomedical Research Excellence (COBRE) and Center for Neurodegeneration and Translational Neuroscience (CNTN)</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kinney, Jefferson W.</creatorcontrib><creatorcontrib>Bemiller, Shane M.</creatorcontrib><creatorcontrib>Murtishaw, Andrew S.</creatorcontrib><creatorcontrib>Leisgang, Amanda M.</creatorcontrib><creatorcontrib>Salazar, Arnold M.</creatorcontrib><creatorcontrib>Lamb, Bruce T.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Wiley Online Library Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Alzheimer's & dementia : translational research & clinical interventions</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kinney, Jefferson W.</au><au>Bemiller, Shane M.</au><au>Murtishaw, Andrew S.</au><au>Leisgang, Amanda M.</au><au>Salazar, Arnold M.</au><au>Lamb, Bruce T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inflammation as a central mechanism in Alzheimer's disease</atitle><jtitle>Alzheimer's & dementia : translational research & clinical interventions</jtitle><addtitle>Alzheimers Dement (N Y)</addtitle><date>2018</date><risdate>2018</risdate><volume>4</volume><issue>1</issue><spage>575</spage><epage>590</epage><pages>575-590</pages><issn>2352-8737</issn><eissn>2352-8737</eissn><abstract>Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized by cognitive decline and the presence of two core pathologies, amyloid β plaques and neurofibrillary tangles. Over the last decade, the presence of a sustained immune response in the brain has emerged as a third core pathology in AD. The sustained activation of the brain's resident macrophages (microglia) and other immune cells has been demonstrated to exacerbate both amyloid and tau pathology and may serve as a link in the pathogenesis of the disorder. In the following review, we provide an overview of inflammation in AD and a detailed coverage of a number of microglia-related signaling mechanisms that have been implicated in AD. Additional information on microglia signaling and a number of cytokines in AD are also reviewed. We also review the potential connection of risk factors for AD and how they may be related to inflammatory mechanisms.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>30406177</pmid><doi>10.1016/j.trci.2018.06.014</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 2352-8737 |
ispartof | Alzheimer's & dementia : translational research & clinical interventions, 2018, Vol.4 (1), p.575-590 |
issn | 2352-8737 2352-8737 |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6214864 |
source | Wiley Online Library Open Access; DOAJ Directory of Open Access Journals; Wiley Online Library Journals Frontfile Complete; PubMed Central; Alma/SFX Local Collection |
subjects | Alzheimer's disease Cytokines Inflammation Microglia Microglia receptors Special Issue from the Centers of Biomedical Research Excellence (COBRE) and Center for Neurodegeneration and Translational Neuroscience (CNTN) |
title | Inflammation as a central mechanism in Alzheimer's disease |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T21%3A39%3A50IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Inflammation%20as%20a%20central%20mechanism%20in%20Alzheimer's%20disease&rft.jtitle=Alzheimer's%20&%20dementia%20:%20translational%20research%20&%20clinical%20interventions&rft.au=Kinney,%20Jefferson%20W.&rft.date=2018&rft.volume=4&rft.issue=1&rft.spage=575&rft.epage=590&rft.pages=575-590&rft.issn=2352-8737&rft.eissn=2352-8737&rft_id=info:doi/10.1016/j.trci.2018.06.014&rft_dat=%3Cproquest_pubme%3E2131244734%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2131244734&rft_id=info:pmid/30406177&rft_els_id=S2352873718300490&rfr_iscdi=true |