Bartels, Claudia

[["dc.bibliographiccitation.journal","Frontiers in Psychiatry"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Hirschel, Sina"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Manig, Anja"],["dc.contributor.author","Falk, Hannah Sönne"],["dc.contributor.author","Ernst, Marielle"],["dc.contributor.author","Vukovich, Ruth"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Bartels, Claudia"],["dc.date.accessioned","2021-04-14T08:23:48Z"],["dc.date.available","2021-04-14T08:23:48Z"],["dc.date.issued","2020"],["dc.description.abstract","Background IgLON5 disease is an autoimmune disorder that shares neuropathological aspects with a tauopathy. Its clinical spectrum is heterogeneous, and figural memory impairment as an initial phenomenon of IgLON5 syndrome has not yet been described. The rationale of this report is to highlight symptoms related to IgLON5 disease that have not been reported to date. This case report will thereby emphasize how important it is to initiate thorough diagnostic methods including cerebrospinal fluid analysis (CSF) before starting early immunotherapy. Methods We examined a 65-year-old Caucasian male via neuropsychological tests, magnetic resonance imaging (MRI), electroencephalography (EEG), neurography and polysomnography. He also underwent two lumbar punctures from which we determined specific autoantibodies in cerebrospinal (CSF) and peripheral blood (PB). Results The patient presented initially complaining of memory loss, gradual dysphagia and sleeping dysfunction. Neuropsychological testing at first presentation and follow-up revealed subtle figural and working memory impairment. At onset and at his 6-month follow-up, we detected IgLON5 antibodies in CSF and PB. Furthermore, we identified in the CSF a blood–brain barrier disturbance at disease onset and follow-up, and markers of neuroaxonal damage such as mildly elevated phosphorylated Tau-181 protein with 86 pg/ml (normal range ≤ 61 pg/ml) at onset. Three months after his initial presentation, he was suffering from axonal neuropathy and transient ataxia in the extremities. Assuming a definitive autoimmune encephalitis-associated with anti-IgLON5 antibodies, we applied high-dose steroids monthly (1g methylprednisolone i.v. for five consecutive days) and his memory complaints, ataxia of extremities and peripheral neuropathy as well as sleeping dysfunction decreased. Conclusions Our findings broaden IgLON5 disease’s clinical spectrum to include predominant and discrete figural memory impairment together with sleeping dysfunction at disease onset. In addition, our report illustrates how important taking an elaborated diagnostic approach is to assuring an accurate diagnosis and the appropriate therapy if a patient presents with a persisting figural memory impairment and sleeping abnormalities so as to avoid overlooking IgLON5 disease and a potentially poor outcome."],["dc.identifier.doi","10.3389/fpsyt.2020.00576"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17685"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81054"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-0640"],["dc.relation.haserratum","/handle/2/83966"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Figural Memory Impairment in Conjunction With Neuropsychiatric Symptoms in IgLON5 Antibody-Associated Autoimmune Encephalitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Psychiatry"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Fitzner, Dirk"],["dc.date.accessioned","2022-04-01T10:00:39Z"],["dc.date.available","2022-04-01T10:00:39Z"],["dc.date.issued","2022"],["dc.description.abstract","Background Glycine receptor antibody-associated neuropsychiatric disease is currently known to be dominated by the phenotypes stiff-person syndrome and progressive encephalomyelitis entailing rigidity and myoclonus. In our case series we aim to depict the less-often reported feature of cognitive impairment associated with glycine receptor antibodies. Methods We investigated five patients with cognitive impairment varying from mild cognitive impairment to dementia associated with serum glycine receptor antibodies. Mild and major neurocognitive disorders were diagnosed according to the DSM-5 (fifth edition of the Diagnostic and Statistical Manual of Mental Disorders). Neuropsychology via Consortium to Establish a Registry for Alzheimer's Disease (CERAD) testing results, psychopathology data via the Manual for the Assessment and Documentation of Psychopathology in Psychiatry (AMDP), cerebrospinal fluid analysis and magnetic resonance imaging data were retrospectively analyzed from patient files. Results We identified five patients with cognitive impairment as the main neuropsychiatric feature associated with serum glycine receptor antibodies. One patient also presented akinetic rigidity syndrome. The psychopathology comprised disorders of attention and memory, orientation, formal thought, and affect. In addition to suffering deficits in verbal memory function, figural recall, phonematic fluency, and globally deteriorated cognitive function, these patients presented seriously impaired memory recall in particular. Tau protein and phosphorylated tau protein 181 were elevated in 75% of patients. Conclusions Our results suggest that axonal neurodegeneration and especially impaired verbal memory recall in addition to deficits in verbal and figural memory characterize patients with progressive cognitive impairment associated with glycine receptor antibodies. This unresolved issue should be clarified by researchers to discover whether axonal degeneration is merely an age-related phenomenon or one related to glycine-receptor autoantibodies in old age. Cognitive impairment as a neuropsychiatric syndrome of glycine-receptor antibody disease is a potential, conceivable, but so far unproven additional feature requiring deeper large-scale investigations and consideration during differential diagnosis in memory clinics."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3389/fpsyt.2021.778684"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105481"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","1664-0640"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Impaired Verbal Memory Recall in Patients With Axonal Degeneration and Serum Glycine-Receptor Autoantibodies—Case Series"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Aging Neuroscience"],["dc.bibliographiccitation.volume","13"],["dc.contributor.affiliation","Hansen, Niels; 1Department of Psychiatry and Psychotherapy, Göttingen, Germany"],["dc.contributor.affiliation","Singh, Aditya; 1Department of Psychiatry and Psychotherapy, Göttingen, Germany"],["dc.contributor.affiliation","Bartels, Claudia; 1Department of Psychiatry and Psychotherapy, Göttingen, Germany"],["dc.contributor.affiliation","Brosseron, Frederic; 3German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany"],["dc.contributor.affiliation","Buerger, Katharina; 5German Center for Neurodegenerative Diseases (DZNE, Munich), Munich, Germany"],["dc.contributor.affiliation","Cetindag, Arda C.; 7Berlin Institute of Health, Institute of Psychiatry and Psychotherapy, Charité—Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin, Germany"],["dc.contributor.affiliation","Dobisch, Laura; 9German Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany"],["dc.contributor.affiliation","Dechent, Peter; 10MR-Research in Neurology and Psychiatry, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Ertl-Wagner, Birgit B.; 11Institute for Clinical Radiology, Ludwig-Maximilians-University, Munich, Germany"],["dc.contributor.affiliation","Fliessbach, Klaus; 3German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany"],["dc.contributor.affiliation","Haynes, John D.; 12Bernstein Center for Computational Neuroscience, Charité—Universitätsmedizin, Berlin, Germany"],["dc.contributor.affiliation","Heneka, Michael T.; 3German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany"],["dc.contributor.affiliation","Janowitz, Daniel; 6Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Munich, Germany"],["dc.contributor.affiliation","Kilimann, Ingo; 13German Center for Neurodegenerative Diseases (DZNE), Rostock, Germany"],["dc.contributor.affiliation","Laske, Christoph; 15German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany"],["dc.contributor.affiliation","Metzger, Coraline D.; 9German Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany"],["dc.contributor.affiliation","Munk, Matthias H.; 15German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany"],["dc.contributor.affiliation","Peters, Oliver; 7Berlin Institute of Health, Institute of Psychiatry and Psychotherapy, Charité—Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin, Germany"],["dc.contributor.affiliation","Priller, Josef; 8German Center for Neurodegenerative Diseases (DZNE), Berlin, Germany"],["dc.contributor.affiliation","Roy, Nina; 3German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany"],["dc.contributor.affiliation","Scheffler, Klaus; 21Department for Biomedical Magnetic Resonance, University of Tübingen, Tübingen, Germany"],["dc.contributor.affiliation","Schneider, Anja; 3German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany"],["dc.contributor.affiliation","Spottke, Annika; 3German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany"],["dc.contributor.affiliation","Spruth, Eike J.; 8German Center for Neurodegenerative Diseases (DZNE), Berlin, Germany"],["dc.contributor.affiliation","Teipel, Stefan; 13German Center for Neurodegenerative Diseases (DZNE), Rostock, Germany"],["dc.contributor.affiliation","Tscheuschler, Maike; 23Department of Psychiatry and Psychotherapy, University of Cologne, Medical Faculty, Cologne, Germany"],["dc.contributor.affiliation","Vukovich, Ruth; 1Department of Psychiatry and Psychotherapy, Göttingen, Germany"],["dc.contributor.affiliation","Wiltfang, Jens; 1Department of Psychiatry and Psychotherapy, Göttingen, Germany"],["dc.contributor.affiliation","Duezel, Emrah; 9German Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany"],["dc.contributor.affiliation","Jessen, Frank; 23Department of Psychiatry and Psychotherapy, University of Cologne, Medical Faculty, Cologne, Germany"],["dc.contributor.affiliation","Goya-Maldonado, Roberto; 1Department of Psychiatry and Psychotherapy, Göttingen, Germany"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Singh, Aditya"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Brosseron, Frederic"],["dc.contributor.author","Buerger, Katharina"],["dc.contributor.author","Cetindag, Arda C."],["dc.contributor.author","Dobisch, Laura"],["dc.contributor.author","Dechent, Peter"],["dc.contributor.author","Ertl-Wagner, Birgit B."],["dc.contributor.author","Goya-Maldonado, Roberto"],["dc.contributor.author","Fliessbach, Klaus"],["dc.contributor.author","Haynes, John D."],["dc.contributor.author","Heneka, Michael T."],["dc.contributor.author","Janowitz, Daniel"],["dc.contributor.author","Kilimann, Ingo"],["dc.contributor.author","Laske, Christoph"],["dc.contributor.author","Metzger, Coraline D."],["dc.contributor.author","Munk, Matthias H."],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Roy, Nina"],["dc.contributor.author","Scheffler, Klaus"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Spottke, Annika"],["dc.contributor.author","Spruth, Eike J."],["dc.contributor.author","Teipel, Stefan"],["dc.contributor.author","Tscheuschler, Maike"],["dc.contributor.author","Vukovich, Ruth"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Duezel, Emrah"],["dc.contributor.author","Jessen, Frank"],["dc.date.accessioned","2021-06-01T09:42:25Z"],["dc.date.available","2021-06-01T09:42:25Z"],["dc.date.issued","2021"],["dc.date.updated","2022-02-09T13:21:10Z"],["dc.description.abstract","Background: The hippocampus and its subfields (HippSub) are reported to be diminished in patients with Alzheimer's disease (AD), bipolar disorder (BD), and major depressive disorder (MDD). We examined these groups vs healthy controls (HC) to reveal HippSub alterations between diseases. Methods: We segmented 3T-MRI T2-weighted hippocampal images of 67 HC, 58 BD, and MDD patients from the AFFDIS study and 137 patients from the DELCODE study assessing cognitive decline, including subjective cognitive decline (SCD), amnestic mild cognitive impairment (aMCI), and AD, via Free Surfer 6.0 to compare volumes across groups. Results: Groups differed significantly in several HippSub volumes, particularly between patients with AD and mood disorders. In comparison to HC, significant lower volumes appear in aMCI and AD groups in specific subfields. Smaller volumes in the left presubiculum are detected in aMCI and AD patients, differing from the BD group. A significant linear regression is seen between left hippocampus volume and duration since the first depressive episode. Conclusions: HippSub volume alterations were observed in AD, but not in early-onset MDD and BD, reinforcing the notion of different neural mechanisms in hippocampal degeneration. Moreover, duration since the first depressive episode was a relevant factor explaining the lower left hippocampal volumes present in groups."],["dc.identifier.doi","10.3389/fnagi.2021.626974"],["dc.identifier.eissn","1663-4365"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85247"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1663-4365"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Hippocampal and Hippocampal-Subfield Volumes From Early-Onset Major Depression and Bipolar Disorder to Cognitive Decline"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Psychiatry"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Timäus, Charles"],["dc.date.accessioned","2021-08-12T07:45:48Z"],["dc.date.available","2021-08-12T07:45:48Z"],["dc.date.issued","2021"],["dc.description.abstract","Flotillin proteins are involved in neurodegeneration and T-cell immunity. Here, we report the case of 65-year-old woman who presented with dementia, depressive symptoms, and a patient history involving speech problems. As diagnostics methods we applied magnetic resonance imaging, clinical examination, extensive neuropsychological testing, and cerebrospinal fluid analysis. Neuropsychological testing revealed major cognitive decline in attentional, executive, and memory functions together with impaired activities of daily living. The cerebrospinal fluid showed elevated phosphorylated tau protein 181. We identified serum autoantibodies against the flotillin 1/2 complex. Immunotherapy entailing four cycles of high-dose steroids resulted in less cognitive dysfunction along with reduced depressive symptoms in the second follow-up after starting steroids. In conclusion: probable autoimmune-mediated dementia associated with anti-flotillin 1/2 complex autoantibodies expands the phenotypic spectrum of anti-flotillin 1/2 antibody disease."],["dc.description.abstract","Flotillin proteins are involved in neurodegeneration and T-cell immunity. Here, we report the case of 65-year-old woman who presented with dementia, depressive symptoms, and a patient history involving speech problems. As diagnostics methods we applied magnetic resonance imaging, clinical examination, extensive neuropsychological testing, and cerebrospinal fluid analysis. Neuropsychological testing revealed major cognitive decline in attentional, executive, and memory functions together with impaired activities of daily living. The cerebrospinal fluid showed elevated phosphorylated tau protein 181. We identified serum autoantibodies against the flotillin 1/2 complex. Immunotherapy entailing four cycles of high-dose steroids resulted in less cognitive dysfunction along with reduced depressive symptoms in the second follow-up after starting steroids. In conclusion: probable autoimmune-mediated dementia associated with anti-flotillin 1/2 complex autoantibodies expands the phenotypic spectrum of anti-flotillin 1/2 antibody disease."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3389/fpsyt.2021.626121"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88553"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.relation.eissn","1664-0640"],["dc.rights","CC BY 4.0"],["dc.title","Case Report: Anti-flotillin 1/2 Autoantibody-Associated Atypical Dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Neurology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.affiliation","Hansen, Niels; 1Department of Psychiatry and Psychotherapy, University Medical Center Goettingen, Göttingen, Germany"],["dc.contributor.affiliation","Malchow, Berend; 1Department of Psychiatry and Psychotherapy, University Medical Center Goettingen, Göttingen, Germany"],["dc.contributor.affiliation","Teegen, Bianca; 2Euroimmun Laboratory, Lübeck, Germany"],["dc.contributor.affiliation","Wiltfang, Jens; 1Department of Psychiatry and Psychotherapy, University Medical Center Goettingen, Göttingen, Germany"],["dc.contributor.affiliation","Bartels, Claudia; 1Department of Psychiatry and Psychotherapy, University Medical Center Goettingen, Göttingen, Germany"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Malchow, Berend"],["dc.contributor.author","Teegen, Bianca"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Bartels, Claudia"],["dc.date.accessioned","2022-06-30T09:44:18Z"],["dc.date.available","2022-06-30T09:44:18Z"],["dc.date.issued","2022-06-16"],["dc.date.updated","2022-06-30T09:37:56Z"],["dc.description.abstract","Background Neurochondrin autoimmunity is a rare disorder mainly associated with cerebellar and vestibular syndromes. Our report aims to enlarge its phenotypic spectrum to encompass major cognitive disorder with very late onset never before reported in conjunction with neurochondrin antibodies. Methods We describe the case of an 85-year-old woman who presented in our memory clinic. Retrospective analysis of patient records included cerebrospinal fluid (CSF) analysis, magnetic resonance imaging (MRI), and neuropsychological testing using the CERAD-plus. Results Because of her unknown onset of progressive cognitive dysfunction in conjunction with speech and language problems, we decided to take an extensive differential diagnostic approach including a search for neural autoantibodies potentially involved in cognitive impairment. Our patient presented serum and CSF neurochondrin autoantibodies. Further CSF analysis revealed elevated tau and ptau 181 protein as well as a reduced Aß42/40 ratio in CSF, thus matching a biomarker profile of Alzheimer's disease (AD). Neuropsychological tests revealed predominant and severe deficits in verbal and visual memory. Her MRI showed reduced parietal and cerebellar brain volume. Discussion Taken together, this case reveals the novelty of a patient with a CSF-based and typical clinical and imaging profile of AD. She is also likely to have neurochondrin autoimmunity, as we detected neurochondrin autoantibodies in her CSF; we therefore diagnosed AD dementia associated with neurochondrin antibodies. Our case expands the spectrum of neurochondrin autoimmunity to disorders involving major cognitive disorder such as AD dementia. Furthermore, we speculate that neurochondrin autoimmunity might have triggered an acceleration of AD symptoms as its onset was reported only after a short 6-month interval via a synergistic or negatively additive hybrid mechanism of action between neurodegeneration and autoimmunity."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3389/fneur.2022.879009"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/111910"],["dc.language.iso","en"],["dc.relation.eissn","1664-2295"],["dc.rights","CC BY 4.0"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Case Report: Alzheimer's Dementia Associated With Cerebrospinal Fluid Neurochondrin Autoantibodies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","760021"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","12"],["dc.contributor.affiliation","Hansen, Niels; \r\n1\r\nDepartment of Psychiatry and Psychotherapy, University Medical Center Goettingen, Goettingen, Germany"],["dc.contributor.affiliation","Stöcker, Winfried; \r\n2\r\nEuroimmun Reference Laboratory, Luebeck, Germany"],["dc.contributor.affiliation","Wiltfang, Jens; \r\n1\r\nDepartment of Psychiatry and Psychotherapy, University Medical Center Goettingen, Goettingen, Germany"],["dc.contributor.affiliation","Bartels, Claudia; \r\n1\r\nDepartment of Psychiatry and Psychotherapy, University Medical Center Goettingen, Goettingen, Germany"],["dc.contributor.affiliation","Rentzsch, Kristin; \r\n2\r\nEuroimmun Reference Laboratory, Luebeck, Germany"],["dc.contributor.affiliation","Bouter, Caroline; \r\n5\r\nDepartment of Nuclear Medicine, University Medical Center Göttingen, Goettingen, Germany"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Rentzsch, Kristin"],["dc.contributor.author","Bouter, Caroline"],["dc.date.accessioned","2022-02-01T10:31:39Z"],["dc.date.available","2022-02-01T10:31:39Z"],["dc.date.issued","2022"],["dc.date.updated","2022-02-09T13:19:47Z"],["dc.description.abstract","Background Frontotemporal lobar degeneration is a heterogeneous disorder entailing a semantic variant of primary progressive aphasia (svPPA). A subtype of frontotemporal dementia associated with glutamate receptor subunit 3 (GluA3) antibody of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) was recently identified. Here, we describe the novelty of a svPPA associated with anti-glial fibrillary acid protein (GFAP) antibodies. Methods To diagnose this 68-year-old woman we conducted a clinical examination, neuropsychological testing, CSF analysis, MRI and 18F-fluorodeoxyglucose (18F-FDG) Positron Emission Tomography (PET)/computed tomography (CT) imaging. Results The clinical phenotype corresponds to a svPPA based on impaired confrontation naming and single-word comprehension. In addition, we observed spared speech production, impaired object knowledge, and surface dyslexia - further supporting the diagnosis of svPPA. Additional characteristic imaging features such as anterior temporal hypometabolism in 18F-FDG PET/CT confirmed patient’s svPPA diagnosis. CSF analysis revealed signs of axonal degeneration, as both tau and phosphorylated tau proteins exceeded normal levels. Her serum showed anti-GFAP autoantibodies. Conclusion We diagnosed a svPPA in this patient and report an association between serum anti-GFAP antibodies and svPPA never reported in the literature so far, thereby expanding the clinical spectrum of svPPA and anti-GFAP-antibody related disease. Further research is needed to elucidate the underlying immunopathology of this disease entity to ultimately improve treatment."],["dc.description.sponsorship","Georg-August-Universität Göttingen"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3389/fimmu.2021.760021"],["dc.identifier.eissn","1664-3224"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/98914"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-517"],["dc.relation.eissn","1664-3224"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Case Report: Semantic Variant of Primary Progressive Aphasia Associated With Anti-Glial Fibrillary Acid Protein Autoantibodies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","829058"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.affiliation","Hansen, Niels; 1Department of Psychiatry and Psychotherapy, Medical University Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Bartels, Claudia; 1Department of Psychiatry and Psychotherapy, Medical University Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Teegen, Bianca; 2Euroimmun Reference Laboratory, Luebeck, Germany"],["dc.contributor.affiliation","Wiltfang, Jens; 1Department of Psychiatry and Psychotherapy, Medical University Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Malchow, Berend; 1Department of Psychiatry and Psychotherapy, Medical University Center Göttingen, Göttingen, Germany"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Teegen, Bianca"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Malchow, Berend"],["dc.date.accessioned","2022-02-23T12:41:58Z"],["dc.date.available","2022-02-23T12:41:58Z"],["dc.date.issued","2022"],["dc.date.updated","2022-03-01T07:15:30Z"],["dc.description.abstract","Background GAD65 autoimmunity is reported to be associated with schizophrenia and bipolar disorder. However, there has been no evidence that glutamic acid decarboxylase 65 (GAD65) autoantibodies in cerebrospinal fluid (CSF) are associated with akinetic catatonia in schizophrenia patients. Methods We report the case of a 28-year-old man who underwent diagnostics including brain MRI, neuropsychological testing, and electroencephalography (EEG) as well as a tumor search via CT of the abdomen and thorax, as well as colonoscopy and gastroscopy. For clinical characterization, his patient files were retrospectively examined. Results Our patient presented catatonia that responded somewhat to benzodiazepines in combination with previously taken antipsychotics such as risperidone for prediagnosed paranoid schizophrenia. Diagnostics revealed GAD65 autoantibodies in his serum and CSF. MRI revealed no brain lesion, and the tumor search had no malignancy. We diagnosed catatonic schizophrenia. Furthermore, as he had not fully recovered, he was given immunotherapy entailing two cycles of intravenous immunoglobulins. Subsequent neuropsychological testing due to subjective cognitive complaints after immunotherapy revealed no objective cognitive deficits. Conclusions We present the novel finding of an association between GAD65 autoantibodies in the serum and CSF with catatonia in a patient suffering from prediagnosed chronic schizophrenia. Due to the presence of CSF GAD65 antibodies and the catatonia factor in prediagnosed schizophrenia, we suspect that his catatonia has an autoimmune origin. Immunotherapy stabilized the catatonia that had initially responded to lorazepam treatment. Further research should be done to characterize patients’ responses to immunotherapy and standard treatment in a large cohort of patients with GAD65 antibody-associated catatonia and schizophrenia."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3389/fimmu.2022.829058"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/100352"],["dc.language.iso","en"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-3224"],["dc.relation.issn","1664-3224"],["dc.rights","CC BY 4.0"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Catatonic Schizophrenia Associated With Cerebrospinal GAD65 Autoantibodies: Case Report and Literature Review"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Psychiatry"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Hirschel, Sina"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Manig, Anja"],["dc.contributor.author","Falk, Hannah Sönne"],["dc.contributor.author","Ernst, Marielle"],["dc.contributor.author","Vukovich, Ruth"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Bartels, Claudia"],["dc.date.accessioned","2021-04-14T08:32:37Z"],["dc.date.available","2021-04-14T08:32:37Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.3389/fpsyt.2020.589466"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83966"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1664-0640"],["dc.relation.iserratumof","/handle/2/81054"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Corrigendum: Figural Memory Impairment in Conjunction With Neuropsychiatric Symptoms in IgLON5 Antibody-Associated Autoimmune Encephalitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","erratum_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","15"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Brain Sciences"],["dc.bibliographiccitation.volume","12"],["dc.contributor.affiliation","Hansen, Niels; 1Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Von-Siebold-Str. 5, 37075 Goettingen, Germany; claudia.bartels@med.uni-goettingen.de"],["dc.contributor.affiliation","Bartels, Claudia; 1Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Von-Siebold-Str. 5, 37075 Goettingen, Germany; claudia.bartels@med.uni-goettingen.de"],["dc.contributor.affiliation","Rentzsch, Kristin; 2Euroimmun Reference Laboratory, Seekamp 31, 23650 Luebeck, Germany; k.rentzsch@euroimmun.de (K.R.); w.stoecker@euroimmun.de (W.S.)"],["dc.contributor.affiliation","Stöcker, Winfried; 2Euroimmun Reference Laboratory, Seekamp 31, 23650 Luebeck, Germany; k.rentzsch@euroimmun.de (K.R.); w.stoecker@euroimmun.de (W.S.)"],["dc.contributor.affiliation","Fitzner, Dirk; 3Department of Neurology, University Medical Center of Goettingen, Robert-Koch Str. 40, 37075 Goettingen, Germany; dirk.fitzner@med.uni-goettingen.de"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Rentzsch, Kristin"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Fitzner, Dirk"],["dc.date.accessioned","2022-02-01T10:31:44Z"],["dc.date.available","2022-02-01T10:31:44Z"],["dc.date.issued","2021"],["dc.date.updated","2022-02-09T13:20:08Z"],["dc.description.abstract","Recoverin-antibody-related disease is currently restricted to late-onset ataxia and autoimmune retinopathy, which can be paraneoplastic or not. However, cognitive dysfunction associated with recoverin antibodies has not been reported so far in a homogeneous patient group. Our case series is dedicated to describing the novel phenotype of cognitive impairment associated with recoverin antibodies. We included five patients with cognitive impairment who presented serum recoverin autoantibodies detected by immunoblots in our case series investigation. We also analyzed their psychopathology, clinical data, cerebrospinal fluid (CSF), and neuroimaging data. Five patients with cognitive impairment associated with serum recoverin antibodies exhibited profound dysfunctional learning and verbal memory. In the CSF of 40% of them, we also diagnosed axonal neurodegeneration entailing elevated tau and phosphorylated tau protein levels. Psychopathologies such as affective symptoms (restlessness, depressive mood, anxiety, complaintiveness) and formal thought disorder, such as rumination, were detected in 25–75% of the patients. We hypothesized a role of recoverin autoimmunity in the pineal gland involving consecutive modulation of hippocampus-based memory caused by an altered release of melatonin. We describe a novel phenotype of possible recoverin autoimmunity in patients with cognitive impairment. However, no clear diagnostic clues can be extracted because of the low diagnostic validity of the testing strategies applied. The possibility of recoverin antibody autoimmunity in the pineal gland correlating with a modulation of hippocampus-based memory should be further investigated."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3390/brainsci12010015"],["dc.identifier.eissn","2076-3425"],["dc.identifier.pii","brainsci12010015"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/98935"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-517"],["dc.relation.eissn","2076-3425"],["dc.rights","CC BY 4.0"],["dc.title","Dysfunctional Learning and Verbal Memory in Patients with Elevated Tau Protein Levels and Serum Recoverin Autoantibodies—Case Series and Review"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1208"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Brain Sciences"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Fitzner, Dirk"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Bartels, Claudia"],["dc.date.accessioned","2021-10-01T09:58:41Z"],["dc.date.available","2021-10-01T09:58:41Z"],["dc.date.issued","2021"],["dc.description.abstract","Background: Chronic traumatic brain injury is a condition that predisposes the brain to activate B-cells and produce neural autoantibodies. Anti-adaptor protein 3, subunit B2 (AP3B2) autoantibodies have thus far been associated with diseases affecting the cerebellum or vestibulocerebellum. Through this case report, we aim to broaden the spectrum of anti-AP3B2-associated disease. Case description: We report on a 51-year-old woman with a brain injury approximately 28 years ago who recently underwent neuropsychological testing, magnetic resonance imaging of the brain (cMRI), and cerebrospinal fluid (CSF) analysis. Neural autoantibodies were determined in serum and CSF. Our patient suffered from mild cognitive impairment (amnestic MCI, multiple domains) with stable memory deficits and a decline in verbal fluency and processing speed within a two-year interval after the first presentation in our memory clinic. Brain MRI showed brain damage in the right temporoparietal, frontolateral region and thalamus, as well as in the left posterior border of the capsula interna and white matter in the frontal region. Since the brain damage, she suffered paresis of the upper extremities on the left side and lower extremities on the right side as well as gait disturbance. Our search for autoantibodies revealed anti-AP3B2 autoantibodies in serum. Conclusions: Our report expands the spectrum of symptoms to mild cognitive impairment in addition to a gait disturbance associated with anti-AP3B2 autoantibodies. Furthermore, it is conceivable that a prior traumatic brain injury could initiate the development of anti-AP3B2-antibody-associated brain autoimmunity, reported here for the first time."],["dc.description.abstract","Background: Chronic traumatic brain injury is a condition that predisposes the brain to activate B-cells and produce neural autoantibodies. Anti-adaptor protein 3, subunit B2 (AP3B2) autoantibodies have thus far been associated with diseases affecting the cerebellum or vestibulocerebellum. Through this case report, we aim to broaden the spectrum of anti-AP3B2-associated disease. Case description: We report on a 51-year-old woman with a brain injury approximately 28 years ago who recently underwent neuropsychological testing, magnetic resonance imaging of the brain (cMRI), and cerebrospinal fluid (CSF) analysis. Neural autoantibodies were determined in serum and CSF. Our patient suffered from mild cognitive impairment (amnestic MCI, multiple domains) with stable memory deficits and a decline in verbal fluency and processing speed within a two-year interval after the first presentation in our memory clinic. Brain MRI showed brain damage in the right temporoparietal, frontolateral region and thalamus, as well as in the left posterior border of the capsula interna and white matter in the frontal region. Since the brain damage, she suffered paresis of the upper extremities on the left side and lower extremities on the right side as well as gait disturbance. Our search for autoantibodies revealed anti-AP3B2 autoantibodies in serum. Conclusions: Our report expands the spectrum of symptoms to mild cognitive impairment in addition to a gait disturbance associated with anti-AP3B2 autoantibodies. Furthermore, it is conceivable that a prior traumatic brain injury could initiate the development of anti-AP3B2-antibody-associated brain autoimmunity, reported here for the first time."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3390/brainsci11091208"],["dc.identifier.pii","brainsci11091208"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/90118"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-469"],["dc.relation.eissn","2076-3425"],["dc.relation.orgunit","Klinik für Psychiatrie und Psychotherapie"],["dc.rights","CC BY 4.0"],["dc.title","Mild Cognitive Impairment in Chronic Brain Injury Associated with Serum Anti-AP3B2 Autoantibodies: Report and Literature Review"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]