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000140669 041__ $$aEnglish
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000140669 1001_ $$0P:(DE-2719)2811131$$aWenke, Nina Kerstin$$b0$$eFirst author$$udzne
000140669 245__ $$aN-methyl-D-aspartate receptor dysfunction by unmutated human antibodies against the NR1 subunit.
000140669 260__ $$aHoboken, NJ$$bWiley-Blackwell$$c2019
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000140669 520__ $$aAnti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is the most common autoimmune encephalitis related to autoantibody-mediated synaptic dysfunction. Cerebrospinal fluid-derived human monoclonal NR1 autoantibodies showed low numbers of somatic hypermutations or were unmutated. These unexpected germline-configured antibodies showed weaker binding to the NMDAR than matured antibodies from the same patient. In primary hippocampal neurons, germline NR1 autoantibodies strongly and specifically reduced total and synaptic NMDAR currents in a dose- and time-dependent manner. The findings suggest that functional NMDAR antibodies are part of the human naïve B cell repertoire. Given their effects on synaptic function, they might contribute to a broad spectrum of neuropsychiatric symptoms. Ann Neurol 2019;85:771-776.
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000140669 650_2 $$2MeSH$$aAnimals
000140669 650_2 $$2MeSH$$aAnti-N-Methyl-D-Aspartate Receptor Encephalitis: blood
000140669 650_2 $$2MeSH$$aAnti-N-Methyl-D-Aspartate Receptor Encephalitis: pathology
000140669 650_2 $$2MeSH$$aAutoantibodies: blood
000140669 650_2 $$2MeSH$$aHEK293 Cells
000140669 650_2 $$2MeSH$$aHippocampus: chemistry
000140669 650_2 $$2MeSH$$aHippocampus: metabolism
000140669 650_2 $$2MeSH$$aHippocampus: pathology
000140669 650_2 $$2MeSH$$aHumans
000140669 650_2 $$2MeSH$$aMice
000140669 650_2 $$2MeSH$$aNeurons: chemistry
000140669 650_2 $$2MeSH$$aNeurons: metabolism
000140669 650_2 $$2MeSH$$aProtein Binding: physiology
000140669 650_2 $$2MeSH$$aProtein Structure, Secondary
000140669 650_2 $$2MeSH$$aReceptors, N-Methyl-D-Aspartate: blood
000140669 650_2 $$2MeSH$$aReceptors, N-Methyl-D-Aspartate: chemistry
000140669 7001_ $$0P:(DE-2719)2811468$$aKreye, Jakob$$b1$$udzne
000140669 7001_ $$0P:(DE-2719)2811708$$aAndrzejak, Ewa$$b2$$udzne
000140669 7001_ $$0P:(DE-2719)2814218$$aCasteren, Adriana$$b3$$udzne
000140669 7001_ $$0P:(DE-2719)2811472$$aLeubner, Jonas$$b4$$udzne
000140669 7001_ $$0P:(DE-HGF)0$$aMurgueitio, Manuela S$$b5
000140669 7001_ $$0P:(DE-2719)2812526$$aReincke, S Momsen$$b6$$udzne
000140669 7001_ $$0P:(DE-2719)9000380$$aSecker, Christopher$$b7$$udzne
000140669 7001_ $$0P:(DE-HGF)0$$aSchmidl, Lars$$b8
000140669 7001_ $$0P:(DE-HGF)0$$aGeis, Christian$$b9
000140669 7001_ $$0P:(DE-2719)2810967$$aAckermann, Frauke$$b10$$udzne
000140669 7001_ $$0P:(DE-HGF)0$$aNikolaus, Marc$$b11
000140669 7001_ $$0P:(DE-2719)2810922$$aGarner, Craig C$$b12$$udzne
000140669 7001_ $$0P:(DE-HGF)0$$aWardemann, Hedda$$b13
000140669 7001_ $$0P:(DE-HGF)0$$aWolber, Gerhard$$b14
000140669 7001_ $$0P:(DE-2719)2810931$$aPrüss, Harald$$b15$$eLast author$$udzne
000140669 77318 $$2Crossref$$3journal-article$$a10.1002/ana.25460$$b : Wiley, 2019-04-02$$n5$$p771-776$$tAnnals of Neurology$$v85$$x0364-5134$$y2019
000140669 773__ $$0PERI:(DE-600)2037912-2$$a10.1002/ana.25460$$gVol. 85, no. 5, p. 771 - 776$$n5$$p771-776$$q85:5<771 - 776$$tAnnals of neurology$$v85$$x0364-5134$$y2019
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