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TREM2 in Alzheimer's Disease: Microglial Survival and Energy Metabolism
Alzheimer's disease (AD) is the leading cause of age-related dementia among the elderly population. Recent genetic studies have identified rare variants of the gene encoding the triggering receptor expressed on myeloid cells-2 (TREM2) as significant genetic risk factors in late-onset AD (LOAD)....
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Published in: | Frontiers in aging neuroscience 2018-11, Vol.10, p.395-395 |
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description | Alzheimer's disease (AD) is the leading cause of age-related dementia among the elderly population. Recent genetic studies have identified rare variants of the gene encoding the triggering receptor expressed on myeloid cells-2 (TREM2) as significant genetic risk factors in late-onset AD (LOAD). TREM2 is specifically expressed in brain microglia and modulates microglial functions in response to key AD pathologies such as amyloid-β (Aβ) plaques and tau tangles. In this review article, we discuss recent research progress in our understanding on the role of TREM2 in microglia and its relevance to AD pathologies. In addition, we discuss evidence describing new TREM2 ligands and the role of TREM2 signaling in microglial survival and energy metabolism. A comprehensive understanding of TREM2 function in the pathogenesis of AD offers a unique opportunity to explore the potential of this microglial receptor as an alternative target in AD therapy. |
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Recent genetic studies have identified rare variants of the gene encoding the triggering receptor expressed on myeloid cells-2 (TREM2) as significant genetic risk factors in late-onset AD (LOAD). TREM2 is specifically expressed in brain microglia and modulates microglial functions in response to key AD pathologies such as amyloid-β (Aβ) plaques and tau tangles. In this review article, we discuss recent research progress in our understanding on the role of TREM2 in microglia and its relevance to AD pathologies. In addition, we discuss evidence describing new TREM2 ligands and the role of TREM2 signaling in microglial survival and energy metabolism. A comprehensive understanding of TREM2 function in the pathogenesis of AD offers a unique opportunity to explore the potential of this microglial receptor as an alternative target in AD therapy.</description><identifier>ISSN: 1663-4365</identifier><identifier>EISSN: 1663-4365</identifier><identifier>DOI: 10.3389/fnagi.2018.00395</identifier><identifier>PMID: 30532704</identifier><language>eng</language><publisher>Switzerland: Frontiers Research Foundation</publisher><subject>Age ; Aging ; Alzheimer's disease ; Amyloid ; Brain research ; Dementia ; Dementia disorders ; Disease ; Energy metabolism ; Geriatrics ; Metabolism ; Microglia ; Myeloid cells ; Neuroscience ; Pathogenesis ; Pathology ; Peptides ; Population genetics ; Population studies ; Proteins ; Risk factors ; Roles ; Senile plaques ; survival ; Tau protein ; TREM2</subject><ispartof>Frontiers in aging neuroscience, 2018-11, Vol.10, p.395-395</ispartof><rights>2018. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Copyright © 2018 Zheng, Cheng, Li, Li, Chen and Zhang. 2018 Zheng, Cheng, Li, Li, Chen and Zhang</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-dce9a22786db6000479a16a4d36077792f42f1717e3844ff97fd0ffdb006ea503</citedby><cites>FETCH-LOGICAL-c490t-dce9a22786db6000479a16a4d36077792f42f1717e3844ff97fd0ffdb006ea503</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2300633075/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2300633075?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,883,25736,27907,27908,36995,36996,44573,53774,53776,74877</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30532704$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zheng, Honghua</creatorcontrib><creatorcontrib>Cheng, Baoying</creatorcontrib><creatorcontrib>Li, Yanfang</creatorcontrib><creatorcontrib>Li, Xin</creatorcontrib><creatorcontrib>Chen, Xiaofen</creatorcontrib><creatorcontrib>Zhang, Yun-Wu</creatorcontrib><title>TREM2 in Alzheimer's Disease: Microglial Survival and Energy Metabolism</title><title>Frontiers in aging neuroscience</title><addtitle>Front Aging Neurosci</addtitle><description>Alzheimer's disease (AD) is the leading cause of age-related dementia among the elderly population. Recent genetic studies have identified rare variants of the gene encoding the triggering receptor expressed on myeloid cells-2 (TREM2) as significant genetic risk factors in late-onset AD (LOAD). TREM2 is specifically expressed in brain microglia and modulates microglial functions in response to key AD pathologies such as amyloid-β (Aβ) plaques and tau tangles. In this review article, we discuss recent research progress in our understanding on the role of TREM2 in microglia and its relevance to AD pathologies. In addition, we discuss evidence describing new TREM2 ligands and the role of TREM2 signaling in microglial survival and energy metabolism. A comprehensive understanding of TREM2 function in the pathogenesis of AD offers a unique opportunity to explore the potential of this microglial receptor as an alternative target in AD therapy.</description><subject>Age</subject><subject>Aging</subject><subject>Alzheimer's disease</subject><subject>Amyloid</subject><subject>Brain research</subject><subject>Dementia</subject><subject>Dementia disorders</subject><subject>Disease</subject><subject>Energy metabolism</subject><subject>Geriatrics</subject><subject>Metabolism</subject><subject>Microglia</subject><subject>Myeloid cells</subject><subject>Neuroscience</subject><subject>Pathogenesis</subject><subject>Pathology</subject><subject>Peptides</subject><subject>Population genetics</subject><subject>Population studies</subject><subject>Proteins</subject><subject>Risk factors</subject><subject>Roles</subject><subject>Senile plaques</subject><subject>survival</subject><subject>Tau protein</subject><subject>TREM2</subject><issn>1663-4365</issn><issn>1663-4365</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpdkc9rFDEUx4MottTePcmAB3vZ9eX3jAeh1G0tdBG0nkNmkkyzZCY1mVmof33T3Vpac8nj5fu-fPM-CL3HsKS0bj67Ufd-SQDXSwDa8FfoEAtBF4wK_vpZfYCOc95AOZQC8PotOqDAKZHADtHF9c_VmlR-rE7D3xvrB5s-5eqbz1Zn-6Va-y7FPngdql9z2vptKfRoqtVoU39Xre2k2xh8Ht6hN06HbI8f7yP0-3x1ffZ9cfXj4vLs9GrRsQamhelsowmRtTCtKImYbDQWmhkqQErZEMeIwxJLS2vGnGukM-CcaQGE1RzoEbrc-5qoN-o2-UGnOxW1V7tGTL3SafJdsKqllmvXMW6kY0yYmtdOOi1kTS2pBSteX_det3M72BJtnJIOL0xfvoz-RvVxqwQRnGJSDE4eDVL8M9s8qcHnzoagRxvnrAjmHAtggIv043_STZzTWFalSKEiChrJiwr2qrL1nJN1T2EwqAfoagddPUBXO-hl5MPzTzwN_ENM7wHjdaan</recordid><startdate>20181123</startdate><enddate>20181123</enddate><creator>Zheng, Honghua</creator><creator>Cheng, Baoying</creator><creator>Li, Yanfang</creator><creator>Li, Xin</creator><creator>Chen, Xiaofen</creator><creator>Zhang, Yun-Wu</creator><general>Frontiers Research Foundation</general><general>Frontiers Media S.A</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20181123</creationdate><title>TREM2 in Alzheimer's Disease: Microglial Survival and Energy Metabolism</title><author>Zheng, Honghua ; Cheng, Baoying ; Li, Yanfang ; Li, Xin ; Chen, Xiaofen ; Zhang, Yun-Wu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c490t-dce9a22786db6000479a16a4d36077792f42f1717e3844ff97fd0ffdb006ea503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Age</topic><topic>Aging</topic><topic>Alzheimer's disease</topic><topic>Amyloid</topic><topic>Brain research</topic><topic>Dementia</topic><topic>Dementia disorders</topic><topic>Disease</topic><topic>Energy metabolism</topic><topic>Geriatrics</topic><topic>Metabolism</topic><topic>Microglia</topic><topic>Myeloid cells</topic><topic>Neuroscience</topic><topic>Pathogenesis</topic><topic>Pathology</topic><topic>Peptides</topic><topic>Population genetics</topic><topic>Population studies</topic><topic>Proteins</topic><topic>Risk factors</topic><topic>Roles</topic><topic>Senile plaques</topic><topic>survival</topic><topic>Tau protein</topic><topic>TREM2</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zheng, Honghua</creatorcontrib><creatorcontrib>Cheng, Baoying</creatorcontrib><creatorcontrib>Li, Yanfang</creatorcontrib><creatorcontrib>Li, Xin</creatorcontrib><creatorcontrib>Chen, Xiaofen</creatorcontrib><creatorcontrib>Zhang, Yun-Wu</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Frontiers in aging neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zheng, Honghua</au><au>Cheng, Baoying</au><au>Li, Yanfang</au><au>Li, Xin</au><au>Chen, Xiaofen</au><au>Zhang, Yun-Wu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TREM2 in Alzheimer's Disease: Microglial Survival and Energy Metabolism</atitle><jtitle>Frontiers in aging neuroscience</jtitle><addtitle>Front Aging Neurosci</addtitle><date>2018-11-23</date><risdate>2018</risdate><volume>10</volume><spage>395</spage><epage>395</epage><pages>395-395</pages><issn>1663-4365</issn><eissn>1663-4365</eissn><abstract>Alzheimer's disease (AD) is the leading cause of age-related dementia among the elderly population. 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subjects | Age Aging Alzheimer's disease Amyloid Brain research Dementia Dementia disorders Disease Energy metabolism Geriatrics Metabolism Microglia Myeloid cells Neuroscience Pathogenesis Pathology Peptides Population genetics Population studies Proteins Risk factors Roles Senile plaques survival Tau protein TREM2 |
title | TREM2 in Alzheimer's Disease: Microglial Survival and Energy Metabolism |
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