Phagocytic Roles of Glial Cells in Healthy and Diseased Brains

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dc.contributor.authorJung, Yeon Jooko
dc.contributor.authorChung, Won-Sukko
dc.date.accessioned2018-07-24T02:57:56Z-
dc.date.available2018-07-24T02:57:56Z-
dc.date.created2018-02-26-
dc.date.created2018-02-26-
dc.date.issued2018-07-
dc.identifier.citationBIOMOLECULES & THERAPEUTICS, v.26, no.4, pp.350 - 357-
dc.identifier.issn1976-9148-
dc.identifier.urihttp://hdl.handle.net/10203/244543-
dc.description.abstractGlial cells are receiving much attention since they have been recognized as important regulators of many aspects of brain function and disease. Recent evidence has revealed that two different glial cells, astrocytes and microglia, control synapse elimination under normal and pathological conditions via phagocytosis. Astrocytes use the MEGF10 and MERTK phagocytic pathways, and microglia use the classical complement pathway to recognize and eliminate unwanted synapses. Notably, glial phagocytosis also contributes to the clearance of disease-specific protein aggregates, such as β-amyloid, huntingtin, and α-synuclein. Here we reivew recent findings showing that glial cells are active regulators in brain functions through phagocytosis and that changes in glial phagocytosis contribute to the pathogenesis of various neurodegenerative diseases. A better understanding of the cellular and molecular mechanisms of glial phagocytosis in healthy and diseased brains will greatly improve our current approach in treating these diseases.-
dc.languageEnglish-
dc.publisherKOREAN SOC APPLIED PHARMACOLOGY-
dc.subjectAMYOTROPHIC-LATERAL-SCLEROSIS-
dc.subjectAMYLOID-BETA PEPTIDE-
dc.subjectTOLL-LIKE RECEPTORS-
dc.subjectALZHEIMERS-DISEASE-
dc.subjectMICROGLIAL ACTIVATION-
dc.subjectSYNAPSE ELIMINATION-
dc.subjectPARKINSONS-DISEASE-
dc.subjectMUTANT HUNTINGTIN-
dc.subjectALPHA-SYNUCLEIN-
dc.subjectA-BETA-
dc.titlePhagocytic Roles of Glial Cells in Healthy and Diseased Brains-
dc.typeArticle-
dc.identifier.wosid000436498900003-
dc.identifier.scopusid2-s2.0-85049790976-
dc.type.rimsART-
dc.citation.volume26-
dc.citation.issue4-
dc.citation.beginningpage350-
dc.citation.endingpage357-
dc.citation.publicationnameBIOMOLECULES & THERAPEUTICS-
dc.identifier.doi10.4062/biomolther.2017.133-
dc.contributor.localauthorChung, Won-Suk-
dc.contributor.nonIdAuthorJung, Yeon Joo-
dc.description.isOpenAccessN-
dc.type.journalArticleReview-
dc.subject.keywordAuthorPhagocytosis-
dc.subject.keywordAuthorAstrocytes-
dc.subject.keywordAuthorMicroglia-
dc.subject.keywordAuthorSynapse elimination-
dc.subject.keywordAuthorNeurodegenerative disease-
dc.subject.keywordPlusAMYOTROPHIC-LATERAL-SCLEROSIS-
dc.subject.keywordPlusAMYLOID-BETA PEPTIDE-
dc.subject.keywordPlusTOLL-LIKE RECEPTORS-
dc.subject.keywordPlusALZHEIMERS-DISEASE-
dc.subject.keywordPlusMICROGLIAL ACTIVATION-
dc.subject.keywordPlusSYNAPSE ELIMINATION-
dc.subject.keywordPlusPARKINSONS-DISEASE-
dc.subject.keywordPlusMUTANT HUNTINGTIN-
dc.subject.keywordPlusALPHA-SYNUCLEIN-
dc.subject.keywordPlusA-BETA-
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