Microglial TREM2 in amyotrophic lateral sclerosis
Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is an aggressive motor neuron degenerative disease characterized by selective loss of both upper and lower motor neurons. The mechanisms underlying disease initiation and progression are poorly understood. The involvement...
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Veröffentlicht in: | Developmental neurobiology (Hoboken, N.J.) N.J.), 2022-01, Vol.82 (1), p.125-137 |
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description | Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is an aggressive motor neuron degenerative disease characterized by selective loss of both upper and lower motor neurons. The mechanisms underlying disease initiation and progression are poorly understood. The involvement of nonmotor neuraxis emphasizes the contribution of glial cells in disease progress. Microglia comprise a unique subset of glial cells and are the principal immune cells in the central nervous system (CNS). Triggering receptor expressed on myeloid cell 2 (TREM2) is a surface receptor that, within the CNS, is exclusively expressed on microglia and plays crucial roles in microglial proliferation, migration, activation, metabolism, and phagocytosis. Genetic evidence has linked TREM2 to neurodegenerative diseases including ALS, but its function in ALS pathogenesis is largely unknown. In this review, we summarize how microglial activation, with a specific focus on TREM2 function, affects ALS progression clinically and experimentally. Understanding microglial TREM2 function will help pinpoint the molecular target for ALS treatment. |
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The mechanisms underlying disease initiation and progression are poorly understood. The involvement of nonmotor neuraxis emphasizes the contribution of glial cells in disease progress. Microglia comprise a unique subset of glial cells and are the principal immune cells in the central nervous system (CNS). Triggering receptor expressed on myeloid cell 2 (TREM2) is a surface receptor that, within the CNS, is exclusively expressed on microglia and plays crucial roles in microglial proliferation, migration, activation, metabolism, and phagocytosis. Genetic evidence has linked TREM2 to neurodegenerative diseases including ALS, but its function in ALS pathogenesis is largely unknown. In this review, we summarize how microglial activation, with a specific focus on TREM2 function, affects ALS progression clinically and experimentally. Understanding microglial TREM2 function will help pinpoint the molecular target for ALS treatment.</description><identifier>ISSN: 1932-8451</identifier><identifier>ISSN: 1932-846X</identifier><identifier>EISSN: 1932-846X</identifier><identifier>DOI: 10.1002/dneu.22864</identifier><identifier>PMID: 34874625</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Amyotrophic lateral sclerosis ; Amyotrophic Lateral Sclerosis - genetics ; Amyotrophic Lateral Sclerosis - metabolism ; Amyotrophic Lateral Sclerosis - pathology ; Central nervous system ; Central Nervous System - metabolism ; Disease ; disease‐associated microglia ; Glial cells ; Humans ; Membrane Glycoproteins - genetics ; Membrane Glycoproteins - metabolism ; Microglia ; Microglia - metabolism ; Motor neurons ; Motor Neurons - metabolism ; Neuraxis ; Neurodegenerative diseases ; Neurodegenerative Diseases - genetics ; Neurodegenerative Diseases - metabolism ; Neurodegenerative Diseases - pathology ; Neuronal-glial interactions ; Phagocytosis ; Receptors, Immunologic - genetics ; Receptors, Immunologic - metabolism ; TDP‐43 ; TREM2</subject><ispartof>Developmental neurobiology (Hoboken, N.J.), 2022-01, Vol.82 (1), p.125-137</ispartof><rights>2021 Wiley Periodicals LLC</rights><rights>2021 Wiley Periodicals LLC.</rights><rights>2022 Wiley Periodicals LLC</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4484-50525a118f07e2e0034d45783627923b0e76ad1519ec8c70b38e3c1d9232dd4d3</citedby><cites>FETCH-LOGICAL-c4484-50525a118f07e2e0034d45783627923b0e76ad1519ec8c70b38e3c1d9232dd4d3</cites><orcidid>0000-0001-8019-3380</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fdneu.22864$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fdneu.22864$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,315,781,785,886,1418,1434,27929,27930,45579,45580,46414,46838</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34874625$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xie, Manling</creatorcontrib><creatorcontrib>Zhao, Shunyi</creatorcontrib><creatorcontrib>Bosco, Dale B.</creatorcontrib><creatorcontrib>Nguyen, Aivi</creatorcontrib><creatorcontrib>Wu, Long‐Jun</creatorcontrib><title>Microglial TREM2 in amyotrophic lateral sclerosis</title><title>Developmental neurobiology (Hoboken, N.J.)</title><addtitle>Dev Neurobiol</addtitle><description>Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is an aggressive motor neuron degenerative disease characterized by selective loss of both upper and lower motor neurons. The mechanisms underlying disease initiation and progression are poorly understood. The involvement of nonmotor neuraxis emphasizes the contribution of glial cells in disease progress. Microglia comprise a unique subset of glial cells and are the principal immune cells in the central nervous system (CNS). Triggering receptor expressed on myeloid cell 2 (TREM2) is a surface receptor that, within the CNS, is exclusively expressed on microglia and plays crucial roles in microglial proliferation, migration, activation, metabolism, and phagocytosis. Genetic evidence has linked TREM2 to neurodegenerative diseases including ALS, but its function in ALS pathogenesis is largely unknown. In this review, we summarize how microglial activation, with a specific focus on TREM2 function, affects ALS progression clinically and experimentally. Understanding microglial TREM2 function will help pinpoint the molecular target for ALS treatment.</description><subject>Amyotrophic lateral sclerosis</subject><subject>Amyotrophic Lateral Sclerosis - genetics</subject><subject>Amyotrophic Lateral Sclerosis - metabolism</subject><subject>Amyotrophic Lateral Sclerosis - pathology</subject><subject>Central nervous system</subject><subject>Central Nervous System - metabolism</subject><subject>Disease</subject><subject>disease‐associated microglia</subject><subject>Glial cells</subject><subject>Humans</subject><subject>Membrane Glycoproteins - genetics</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Microglia</subject><subject>Microglia - metabolism</subject><subject>Motor neurons</subject><subject>Motor Neurons - metabolism</subject><subject>Neuraxis</subject><subject>Neurodegenerative diseases</subject><subject>Neurodegenerative Diseases - genetics</subject><subject>Neurodegenerative Diseases - metabolism</subject><subject>Neurodegenerative Diseases - pathology</subject><subject>Neuronal-glial interactions</subject><subject>Phagocytosis</subject><subject>Receptors, Immunologic - genetics</subject><subject>Receptors, Immunologic - metabolism</subject><subject>TDP‐43</subject><subject>TREM2</subject><issn>1932-8451</issn><issn>1932-846X</issn><issn>1932-846X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc1LwzAAxYMobk4v_gFS8CJCZz7b9CLInB-wKcgG3kKWZltG18ykVfbfm9k51IOnBN6Pl5f3ADhFsIsgxFd5qesuxjyhe6CNMoJjTpPX_d2doRY48n4BISM4gYegRShPaYJZG6ChUc7OCiOLaPTSH-LIlJFcrm3l7GpuVFTISrsgelVoZ73xx-BgKguvT7ZnB4zv-qPeQzx4vn_s3QxiRSmnMYMMM4kQn8JUYw0hoTllKScJTjNMJlCnicwRQ5lWXKVwQrgmCuVBw3lOc9IB143vqp4sda50WYUcYuXMUrq1sNKI30pp5mJm3wXnGYfhoQ642Bo4-1ZrX4ml8UoXhSy1rb0IVaSMQ0pxQM__oAtbuzJ8L1AYZ5QlGAXqsqFCY947Pd2FQVBslhCbJcTXEgE--xl_h35XHwDUAB-m0Ot_rMTtU3_cmH4C_0iR-Q</recordid><startdate>202201</startdate><enddate>202201</enddate><creator>Xie, Manling</creator><creator>Zhao, Shunyi</creator><creator>Bosco, Dale B.</creator><creator>Nguyen, Aivi</creator><creator>Wu, Long‐Jun</creator><general>Wiley Subscription Services, 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>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-8019-3380</orcidid></search><sort><creationdate>202201</creationdate><title>Microglial TREM2 in amyotrophic lateral sclerosis</title><author>Xie, Manling ; Zhao, Shunyi ; Bosco, Dale B. ; Nguyen, Aivi ; Wu, Long‐Jun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4484-50525a118f07e2e0034d45783627923b0e76ad1519ec8c70b38e3c1d9232dd4d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Amyotrophic lateral sclerosis</topic><topic>Amyotrophic Lateral Sclerosis - genetics</topic><topic>Amyotrophic Lateral Sclerosis - metabolism</topic><topic>Amyotrophic Lateral Sclerosis - pathology</topic><topic>Central nervous system</topic><topic>Central Nervous System - metabolism</topic><topic>Disease</topic><topic>disease‐associated microglia</topic><topic>Glial cells</topic><topic>Humans</topic><topic>Membrane Glycoproteins - genetics</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Microglia</topic><topic>Microglia - metabolism</topic><topic>Motor neurons</topic><topic>Motor Neurons - metabolism</topic><topic>Neuraxis</topic><topic>Neurodegenerative diseases</topic><topic>Neurodegenerative Diseases - genetics</topic><topic>Neurodegenerative Diseases - metabolism</topic><topic>Neurodegenerative Diseases - pathology</topic><topic>Neuronal-glial interactions</topic><topic>Phagocytosis</topic><topic>Receptors, Immunologic - genetics</topic><topic>Receptors, Immunologic - metabolism</topic><topic>TDP‐43</topic><topic>TREM2</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xie, Manling</creatorcontrib><creatorcontrib>Zhao, Shunyi</creatorcontrib><creatorcontrib>Bosco, Dale B.</creatorcontrib><creatorcontrib>Nguyen, Aivi</creatorcontrib><creatorcontrib>Wu, Long‐Jun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Developmental neurobiology (Hoboken, N.J.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xie, Manling</au><au>Zhao, Shunyi</au><au>Bosco, Dale B.</au><au>Nguyen, Aivi</au><au>Wu, Long‐Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Microglial TREM2 in amyotrophic lateral sclerosis</atitle><jtitle>Developmental neurobiology (Hoboken, N.J.)</jtitle><addtitle>Dev Neurobiol</addtitle><date>2022-01</date><risdate>2022</risdate><volume>82</volume><issue>1</issue><spage>125</spage><epage>137</epage><pages>125-137</pages><issn>1932-8451</issn><issn>1932-846X</issn><eissn>1932-846X</eissn><abstract>Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is an aggressive motor neuron degenerative disease characterized by selective loss of both upper and lower motor neurons. The mechanisms underlying disease initiation and progression are poorly understood. The involvement of nonmotor neuraxis emphasizes the contribution of glial cells in disease progress. Microglia comprise a unique subset of glial cells and are the principal immune cells in the central nervous system (CNS). Triggering receptor expressed on myeloid cell 2 (TREM2) is a surface receptor that, within the CNS, is exclusively expressed on microglia and plays crucial roles in microglial proliferation, migration, activation, metabolism, and phagocytosis. Genetic evidence has linked TREM2 to neurodegenerative diseases including ALS, but its function in ALS pathogenesis is largely unknown. In this review, we summarize how microglial activation, with a specific focus on TREM2 function, affects ALS progression clinically and experimentally. 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subjects | Amyotrophic lateral sclerosis Amyotrophic Lateral Sclerosis - genetics Amyotrophic Lateral Sclerosis - metabolism Amyotrophic Lateral Sclerosis - pathology Central nervous system Central Nervous System - metabolism Disease disease‐associated microglia Glial cells Humans Membrane Glycoproteins - genetics Membrane Glycoproteins - metabolism Microglia Microglia - metabolism Motor neurons Motor Neurons - metabolism Neuraxis Neurodegenerative diseases Neurodegenerative Diseases - genetics Neurodegenerative Diseases - metabolism Neurodegenerative Diseases - pathology Neuronal-glial interactions Phagocytosis Receptors, Immunologic - genetics Receptors, Immunologic - metabolism TDP‐43 TREM2 |
title | Microglial TREM2 in amyotrophic lateral sclerosis |
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