Dahm, Liane

[["dc.bibliographiccitation.firstpage","82"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","94"],["dc.bibliographiccitation.volume","76"],["dc.contributor.author","Dahm, Liane"],["dc.contributor.author","Ott, Christoph"],["dc.contributor.author","Steiner, Johann"],["dc.contributor.author","Stepniak, Beata"],["dc.contributor.author","Teegen, Bianca"],["dc.contributor.author","Saschenbrecker, Sandra"],["dc.contributor.author","Hammer, Christian"],["dc.contributor.author","Borowski, Kathrin"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Lemke, Sandra"],["dc.contributor.author","Rentzsch, Kristin"],["dc.contributor.author","Probst, Christian"],["dc.contributor.author","Martens, Henrik"],["dc.contributor.author","Wienands, Jürgen"],["dc.contributor.author","Spalletta, Gianfranco"],["dc.contributor.author","Weißenborn, Karin"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:34Z"],["dc.date.available","2017-09-07T11:46:34Z"],["dc.date.issued","2014"],["dc.description.abstract","ObjectiveWe previously reported an unexpectedly high seroprevalence (∼10%) of N-methyl-D-aspartate-receptor subunit-NR1 (NMDAR1) autoantibodies (AB) in healthy and neuropsychiatrically ill subjects (N = 2,817). This finding challenges an unambiguous causal relationship of serum AB with brain disease. To test whether similar results would be obtained for other brain antigen-directed AB previously connected with pathological conditions, we systematically screened serum samples of 4,236 individuals.MethodsSerum samples of healthy (n = 1,703) versus neuropsychiatrically ill subjects (schizophrenia, affective disorders, stroke, Parkinson disease, amyotrophic lateral sclerosis, personality disorder; total n = 2,533) were tested. For analysis based on indirect immunofluorescence, we used biochip mosaics of frozen brain sections (rat, monkey) and transfected HEK293 cells expressing respective recombinant target antigens.ResultsSeroprevalence of all screened AB was comparable in healthy and ill individuals. None of them, however, reached the abundance of NMDAR1 AB (again ∼10%; immunoglobulin [Ig] G ∼1%). Appreciable frequency was noted for AB against amphiphysin (2.0%), ARHGAP26 (1.3%), CASPR2 (0.9%), MOG (0.8%), GAD65 (0.5%), Ma2 (0.5%), Yo (0.4%), and Ma1 (0.4%), with titers and Ig class distribution similar among groups. All other AB were found in ≤0.1% of individuals (anti–AMPAR-1/2, AQP4, CV2, Tr/DNER, DPPX-IF1, GABAR-B1/B2, GAD67, GLRA1b, GRM1, GRM5, Hu, LGl1, recoverin, Ri, ZIC4). The predominant Ig class depended on antigen location, with intracellular epitopes predisposing to IgG (chi-square = 218.91, p = 2.8 × 10−48).InterpretationTo conclude, the brain antigen-directed AB tested here are comparably detectable in healthy subjects and the disease groups studied here, thus questioning an upfront pathological role of these serum AB."],["dc.identifier.doi","10.1002/ana.24189"],["dc.identifier.gro","3150539"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7312"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Seroprevalence of autoantibodies against brain antigens in health and disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1180"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Stroke"],["dc.bibliographiccitation.lastpage","1186"],["dc.bibliographiccitation.volume","46"],["dc.contributor.author","Zerche, M."],["dc.contributor.author","Weißenborn, Karin"],["dc.contributor.author","Ott, C."],["dc.contributor.author","Dere, Ekrem"],["dc.contributor.author","Asif, Abdul R."],["dc.contributor.author","Worthmann, Hans"],["dc.contributor.author","Hassouna, I."],["dc.contributor.author","Rentzsch, Katrin"],["dc.contributor.author","Tryc, A. B."],["dc.contributor.author","Dahm, Liane"],["dc.contributor.author","Steiner, Johann"],["dc.contributor.author","Binder, Lutz"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Sirén, A.-L."],["dc.contributor.author","Stöcker, W."],["dc.contributor.author","Ehrenreich, Hanhelore"],["dc.date.accessioned","2017-09-07T11:44:23Z"],["dc.date.available","2017-09-07T11:44:23Z"],["dc.date.issued","2015"],["dc.description.abstract","Background and Purpose—Recently, we reported high seroprevalence (age-dependent up to >19%) of N-methyl-d-aspartate-receptor subunit NR1 (NMDAR1) autoantibodies in both healthy and neuropsychiatrically ill subjects (N=4236). Neuropsychiatric syndrome relevance was restricted to individuals with compromised blood–brain barrier, for example, apolipoprotein E4 (APOE4) carrier status, both clinically and experimentally. We now hypothesized that these autoantibodies may upon stroke be protective in individuals with hitherto intact blood–brain barrier, but harmful for subjects with chronically compromised blood–brain barrier.Methods—Of 464 patients admitted with acute ischemic stroke in the middle cerebral artery territory, blood for NMDAR1 autoantibody measurements and APOE4 carrier status as indicator of a preexisting leaky blood–brain barrier was collected within 3 to 5 hours after stroke. Evolution of lesion size (delta day 7–1) in diffusion-weighted magnetic resonance imaging was primary outcome parameter. In subgroups, NMDAR1 autoantibody measurements were repeated on days 2 and 7.Results—Of all 464 patients, 21.6% were NMDAR1 autoantibody–positive (immunoglobulin M, A, or G) and 21% were APOE4 carriers. Patients with magnetic resonance imaging data available on days 1 and 7 (N=384) were divided into 4 groups according to NMDAR1 autoantibody and APOE4 status. Groups were comparable in all stroke-relevant presenting characteristics. The autoantibody+/APOE4− group had a smaller mean delta lesion size compared with the autoantibody−/APOE4- group, suggesting a protective effect of circulating NMDAR1 autoantibodies. In contrast, the autoantibody+/APOE4+ group had the largest mean delta lesion area. NMDAR1 autoantibody serum titers dropped on day 2 and remounted by day 7.Conclusions—Dependent on blood–brain barrier integrity before an acute ischemic brain injury, preexisting NMDAR1 autoantibodies seem to be beneficial or detrimental."],["dc.identifier.doi","10.1161/strokeaha.114.008323"],["dc.identifier.gro","3151637"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8453"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0039-2499"],["dc.title","Preexisting Serum Autoantibodies Against the NMDAR Subunit NR1 Modulate Evolution of Lesion Size in Acute Ischemic Stroke"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]