Plaque attack by microglial PLCγ2
PLCγ2 is genetically linked to Alzheimer’s disease (AD), but it is unclear how PLCγ2 contributes to pathology. Tsai et al. demonstrate that AD-associated PLCG2 variants bidirectionally orchestrate microglial responses to plaques and impact neural function in an AD mouse model. This positions PLCγ2 a...
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| Veröffentlicht in: | Immunity (Cambridge, Mass.) Mass.), 2023-09, Vol.56 (9), p.1985-1987 |
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| Sprache: | eng |
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| container_end_page | 1987 |
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| container_issue | 9 |
| container_start_page | 1985 |
| container_title | Immunity (Cambridge, Mass.) |
| container_volume | 56 |
| creator | Comer, Ashley L. Hammond, Timothy R. |
| description | PLCγ2 is genetically linked to Alzheimer’s disease (AD), but it is unclear how PLCγ2 contributes to pathology. Tsai et al. demonstrate that AD-associated PLCG2 variants bidirectionally orchestrate microglial responses to plaques and impact neural function in an AD mouse model. This positions PLCγ2 as a key microglial signaling node and shows that targeting PLCγ2 could have therapeutic benefits in AD.
PLCγ2 is genetically linked to Alzheimer’s disease (AD), but it is unclear how PLCγ2 contributes to pathology. Tsai et al. demonstrate that AD-associated PLCG2 variants bidirectionally orchestrate microglial responses to plaques and impact neural function in an AD mouse model. This positions PLCγ2 as a key microglial signaling node and shows that targeting PLCγ2 could have therapeutic benefits in AD. |
| doi_str_mv | 10.1016/j.immuni.2023.08.012 |
| format | Article |
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PLCγ2 is genetically linked to Alzheimer’s disease (AD), but it is unclear how PLCγ2 contributes to pathology. Tsai et al. demonstrate that AD-associated PLCG2 variants bidirectionally orchestrate microglial responses to plaques and impact neural function in an AD mouse model. This positions PLCγ2 as a key microglial signaling node and shows that targeting PLCγ2 could have therapeutic benefits in AD.</description><identifier>ISSN: 1074-7613</identifier><identifier>ISSN: 1097-4180</identifier><identifier>EISSN: 1097-4180</identifier><identifier>DOI: 10.1016/j.immuni.2023.08.012</identifier><language>eng</language><publisher>Elsevier Inc</publisher><ispartof>Immunity (Cambridge, Mass.), 2023-09, Vol.56 (9), p.1985-1987</ispartof><rights>2023 Elsevier Inc.</rights><rights>Copyright © 2023 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c288t-73ee781afff10483be0680fa4040609c98555f47b173634b1a2dd483bce6b74a3</cites><orcidid>0000-0002-7073-892X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1074761323003680$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids></links><search><creatorcontrib>Comer, Ashley L.</creatorcontrib><creatorcontrib>Hammond, Timothy R.</creatorcontrib><title>Plaque attack by microglial PLCγ2</title><title>Immunity (Cambridge, Mass.)</title><description>PLCγ2 is genetically linked to Alzheimer’s disease (AD), but it is unclear how PLCγ2 contributes to pathology. Tsai et al. demonstrate that AD-associated PLCG2 variants bidirectionally orchestrate microglial responses to plaques and impact neural function in an AD mouse model. This positions PLCγ2 as a key microglial signaling node and shows that targeting PLCγ2 could have therapeutic benefits in AD.
PLCγ2 is genetically linked to Alzheimer’s disease (AD), but it is unclear how PLCγ2 contributes to pathology. Tsai et al. demonstrate that AD-associated PLCG2 variants bidirectionally orchestrate microglial responses to plaques and impact neural function in an AD mouse model. This positions PLCγ2 as a key microglial signaling node and shows that targeting PLCγ2 could have therapeutic benefits in AD.</description><issn>1074-7613</issn><issn>1097-4180</issn><issn>1097-4180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNp9kM1KxDAUhYMoOI6-gYviyk3rzU-TdCPI4B8UnIWuQ5omkrGdjklHmOfyPXwmU-ra1T2Lcw7nfghdYigwYH6zKXzf77e-IEBoAbIATI7QAkMlcoYlHE9asFxwTE_RWYwbAMzKChboat3pz73N9Dhq85E1h6z3Jgzvndddtq5XP9_kHJ043UV78XeX6O3h_nX1lNcvj8-ruzo3RMoxF9RaIbF2zmFgkjYWuASnGTDgUJlKlmXpmGiwoJyyBmvStpPPWN4IpukSXc-9uzCkSXFUvY_Gdp3e2mEfFZGcVWk458nKZmuaGmOwTu2C73U4KAxqQqI2akaiJiQKpEpIUux2jtn0xpe3QUXj7dbY1gdrRtUO_v-CXy5UakE</recordid><startdate>20230912</startdate><enddate>20230912</enddate><creator>Comer, Ashley L.</creator><creator>Hammond, Timothy R.</creator><general>Elsevier Inc</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-7073-892X</orcidid></search><sort><creationdate>20230912</creationdate><title>Plaque attack by microglial PLCγ2</title><author>Comer, Ashley L. ; Hammond, Timothy R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c288t-73ee781afff10483be0680fa4040609c98555f47b173634b1a2dd483bce6b74a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Comer, Ashley L.</creatorcontrib><creatorcontrib>Hammond, Timothy R.</creatorcontrib><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Immunity (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Comer, Ashley L.</au><au>Hammond, Timothy R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Plaque attack by microglial PLCγ2</atitle><jtitle>Immunity (Cambridge, Mass.)</jtitle><date>2023-09-12</date><risdate>2023</risdate><volume>56</volume><issue>9</issue><spage>1985</spage><epage>1987</epage><pages>1985-1987</pages><issn>1074-7613</issn><issn>1097-4180</issn><eissn>1097-4180</eissn><abstract>PLCγ2 is genetically linked to Alzheimer’s disease (AD), but it is unclear how PLCγ2 contributes to pathology. Tsai et al. demonstrate that AD-associated PLCG2 variants bidirectionally orchestrate microglial responses to plaques and impact neural function in an AD mouse model. This positions PLCγ2 as a key microglial signaling node and shows that targeting PLCγ2 could have therapeutic benefits in AD.
PLCγ2 is genetically linked to Alzheimer’s disease (AD), but it is unclear how PLCγ2 contributes to pathology. Tsai et al. demonstrate that AD-associated PLCG2 variants bidirectionally orchestrate microglial responses to plaques and impact neural function in an AD mouse model. This positions PLCγ2 as a key microglial signaling node and shows that targeting PLCγ2 could have therapeutic benefits in AD.</abstract><pub>Elsevier Inc</pub><doi>10.1016/j.immuni.2023.08.012</doi><tpages>3</tpages><orcidid>https://orcid.org/0000-0002-7073-892X</orcidid></addata></record> |
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| source | Cell Press Free Archives; Elsevier ScienceDirect Journals; EZB-FREE-00999 freely available EZB journals |
| title | Plaque attack by microglial PLCγ2 |
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