Home > Publications Database > Differential interaction with TREM2 modulates microglial uptake of modified Aβ species. > print

001     162700
005     20250604100729.0
024 7 _ |a 10.1002/glia.24077
|2 doi
024 7 _ |a pmid:34427354
|2 pmid
024 7 _ |a 0894-1491
|2 ISSN
024 7 _ |a 1098-1136
|2 ISSN
024 7 _ |a altmetric:112324279
|2 altmetric
037 _ _ |a DZNE-2021-01357
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Joshi, Pranav
|0 0000-0002-1153-0440
|b 0
245 _ _ |a Differential interaction with TREM2 modulates microglial uptake of modified Aβ species.
260 _ _ |a Bognor Regis [u.a.]
|c 2021
|b Wiley-Liss
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1748938354_19908
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a Rare coding variants of the microglial triggering receptor expressed on myeloid cells 2 (TREM2) confer an increased risk for Alzheimer's disease (AD) characterized by the progressive accumulation of aggregated forms of amyloid β peptides (Aβ). Aβ peptides are generated by proteolytic processing of the amyloid precursor protein (APP). Heterogeneity in proteolytic cleavages and additional post-translational modifications result in the production of several distinct Aβ variants that could differ in their aggregation behavior and toxic properties. Here, we sought to assess whether post-translational modifications of Aβ affect the interaction with TREM2. Biophysical and biochemical methods revealed that TREM2 preferentially interacts with oligomeric Aβ, and that phosphorylation of Aβ increases this interaction. Phosphorylation of Aβ also affected the TREM2 dependent interaction and phagocytosis by primary microglia and in APP transgenic mouse models. Thus, TREM2 function is important for sensing phosphorylated Aβ variants in distinct aggregation states and reduces the accumulation and deposition of these toxic Aβ species in preclinical models of Alzheimer's disease.
536 _ _ |a 353 - Clinical and Health Care Research (POF4-353)
|0 G:(DE-HGF)POF4-353
|c POF4-353
|f POF IV
|x 0
536 _ _ |a 352 - Disease Mechanisms (POF4-352)
|0 G:(DE-HGF)POF4-352
|c POF4-352
|f POF IV
|x 1
536 _ _ |a 899 - ohne Topic (POF4-899)
|0 G:(DE-HGF)POF4-899
|c POF4-899
|f POF IV
|x 2
588 _ _ |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
650 _ 7 |a Alzheimer's disease
|2 Other
650 _ 7 |a FTD mutation
|2 Other
650 _ 7 |a TREM2
|2 Other
650 _ 7 |a amyloid β
|2 Other
650 _ 7 |a phosphorylation
|2 Other
650 _ 7 |a post-translational modification
|2 Other
650 _ 2 |a Alzheimer Disease: genetics
|2 MeSH
650 _ 2 |a Alzheimer Disease: metabolism
|2 MeSH
650 _ 2 |a Amyloid beta-Peptides: metabolism
|2 MeSH
650 _ 2 |a Amyloid beta-Protein Precursor: genetics
|2 MeSH
650 _ 2 |a Amyloid beta-Protein Precursor: metabolism
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Disease Models, Animal
|2 MeSH
650 _ 2 |a Membrane Glycoproteins: genetics
|2 MeSH
650 _ 2 |a Membrane Glycoproteins: metabolism
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Mice, Transgenic
|2 MeSH
650 _ 2 |a Microglia: metabolism
|2 MeSH
650 _ 2 |a Receptors, Immunologic: genetics
|2 MeSH
650 _ 2 |a Receptors, Immunologic: metabolism
|2 MeSH
700 1 _ |a Riffel, Florian
|0 0000-0001-8594-100X
|b 1
700 1 _ |a Satoh, Kanayo
|b 2
700 1 _ |a Enomoto, Masahiro
|b 3
700 1 _ |a Qamar, Seema
|b 4
700 1 _ |a Scheiblich, Hannah
|0 P:(DE-2719)9000371
|b 5
|u dzne
700 1 _ |a Villacampa, Nàdia
|0 P:(DE-2719)9000326
|b 6
|u dzne
700 1 _ |a Kumar, Sathish
|0 0000-0002-2792-7047
|b 7
700 1 _ |a Theil, Sandra
|b 8
700 1 _ |a Parhizkar, Samira
|0 0000-0001-5807-190X
|b 9
700 1 _ |a Haass, Christian
|0 P:(DE-2719)2202037
|b 10
|u dzne
700 1 _ |a Heneka, Michael
|0 P:(DE-2719)2000008
|b 11
|u dzne
700 1 _ |a Fraser, Paul E
|b 12
700 1 _ |a St George-Hyslop, Peter
|b 13
700 1 _ |a Walter, Jochen
|0 P:(DE-HGF)0
|b 14
773 _ _ |a 10.1002/glia.24077
|g Vol. 69, no. 12, p. 2917 - 2932
|0 PERI:(DE-600)1474828-9
|n 12
|p 2917 - 2932
|t Glia
|v 69
|y 2021
|x 1098-1136
856 4 _ |u https://pub.dzne.de/record/162700/files/DZNE-2021-01357.pdf
|y OpenAccess
856 4 _ |u https://pub.dzne.de/record/162700/files/DZNE-2021-01357.pdf?subformat=pdfa
|x pdfa
|y OpenAccess
909 C O |o oai:pub.dzne.de:162700
|p openaire
|p open_access
|p VDB
|p driver
|p dnbdelivery
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 5
|6 P:(DE-2719)9000371
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 6
|6 P:(DE-2719)9000326
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 10
|6 P:(DE-2719)2202037
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 11
|6 P:(DE-2719)2000008
913 1 _ |a DE-HGF
|b Gesundheit
|l Neurodegenerative Diseases
|1 G:(DE-HGF)POF4-350
|0 G:(DE-HGF)POF4-353
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Clinical and Health Care Research
|x 0
913 1 _ |a DE-HGF
|b Gesundheit
|l Neurodegenerative Diseases
|1 G:(DE-HGF)POF4-350
|0 G:(DE-HGF)POF4-352
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Disease Mechanisms
|x 1
913 1 _ |a DE-HGF
|b Programmungebundene Forschung
|l ohne Programm
|1 G:(DE-HGF)POF4-890
|0 G:(DE-HGF)POF4-899
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-800
|4 G:(DE-HGF)POF
|v ohne Topic
|x 2
914 1 _ |y 2021
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
|d 2022-11-08
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
|d 2022-11-08
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
|d 2022-11-08
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1190
|2 StatID
|b Biological Abstracts
|d 2021-01-29
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b GLIA : 2021
|d 2022-11-08
915 _ _ |a Creative Commons Attribution-NonCommercial CC BY-NC 4.0
|0 LIC:(DE-HGF)CCBYNC4
|2 HGFVOC
915 _ _ |a DEAL Wiley
|0 StatID:(DE-HGF)3001
|2 StatID
|d 2021-01-29
|w ger
915 _ _ |a WoS
|0 StatID:(DE-HGF)0113
|2 StatID
|b Science Citation Index Expanded
|d 2021-01-29
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1030
|2 StatID
|b Current Contents - Life Sciences
|d 2022-11-08
915 _ _ |a OpenAccess
|0 StatID:(DE-HGF)0510
|2 StatID
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
|d 2022-11-08
915 _ _ |a IF >= 5
|0 StatID:(DE-HGF)9905
|2 StatID
|b GLIA : 2021
|d 2022-11-08
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0160
|2 StatID
|b Essential Science Indicators
|d 2021-01-29
915 _ _ |a Nationallizenz
|0 StatID:(DE-HGF)0420
|2 StatID
|d 2022-11-08
|w ger
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
|d 2022-11-08
920 1 _ |0 I:(DE-2719)1011301
|k Biomarker
|l Interventional Trials and Biomarkers in Neurodegenerative Diseases
|x 0
920 1 _ |0 I:(DE-2719)1011303
|k AG Heneka
|l Neuroinflammation, Biomarker
|x 1
920 1 _ |0 I:(DE-2719)1110007
|k AG Haass
|l Molecular Neurodegeneration
|x 2
920 1 _ |0 I:(DE-2719)1030028
|k Tech Transfer
|l Technology Transfer and Industry Collaborations Unit
|x 3
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a I:(DE-2719)1011301
980 _ _ |a I:(DE-2719)1011303
980 _ _ |a I:(DE-2719)1110007
980 _ _ |a I:(DE-2719)1030028
980 _ _ |a UNRESTRICTED
980 1 _ |a FullTexts

LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21