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...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Alzheimer's & dementia : translational research & clinical interventions 2018, Vol.4 (1), p.575-590
Hauptverfasser: Kinney, Jefferson W., Bemiller, Shane M., Murtishaw, Andrew S., Leisgang, Amanda M., Salazar, Arnold M., Lamb, Bruce T.
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 &amp; dementia : translational research &amp; 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 &amp; dementia : translational research &amp; 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 &amp; dementia : translational research &amp; 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 &amp; dementia : translational research &amp; 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