Bouter, Caroline

[["dc.bibliographiccitation.firstpage","62"],["dc.bibliographiccitation.journal","Clinica Chimica Acta"],["dc.bibliographiccitation.lastpage","68"],["dc.bibliographiccitation.volume","492"],["dc.contributor.author","Bouter, Caroline"],["dc.contributor.author","Vogelgsang, Jonathan"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2020-12-10T14:22:55Z"],["dc.date.available","2020-12-10T14:22:55Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.cca.2019.02.005"],["dc.identifier.issn","0009-8981"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71778"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Comparison between amyloid-PET and CSF amyloid-β biomarkers in a clinical cohort with memory deficits"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","203"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Alzheimer's Disease"],["dc.bibliographiccitation.lastpage","212"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Vogelgsang, Jonathan"],["dc.contributor.author","Wedekind, Dirk"],["dc.contributor.author","Bouter, Caroline"],["dc.contributor.author","Klafki, Hans-W."],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2020-12-10T18:44:11Z"],["dc.date.available","2020-12-10T18:44:11Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.3233/JAD-170793"],["dc.identifier.eissn","1875-8908"],["dc.identifier.issn","1387-2877"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78359"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Reproducibility of Alzheimer’s Disease Cerebrospinal Fluid-Biomarker Measurements under Clinical Routine Conditions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","815813"],["dc.bibliographiccitation.journal","Frontiers in Aging Neuroscience"],["dc.bibliographiccitation.volume","14"],["dc.contributor.affiliation","Hansen, Niels; 1Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Müller, Sebastian Johannes; 2Institute of Diagnostic and Interventional Neuroradiology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Khadhraoui, Eya; 2Institute of Diagnostic and Interventional Neuroradiology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Riedel, Christian Heiner; 2Institute of Diagnostic and Interventional Neuroradiology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Langer, Philip; 2Institute of Diagnostic and Interventional Neuroradiology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Wiltfang, Jens; 1Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Timäus, Charles-Arnold; 1Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Bouter, Caroline; 5Department of Nuclear Medicine, University Medical Center Göttingen (UMG), Georg August University, Göttingen, Germany"],["dc.contributor.affiliation","Ernst, Marielle; 2Institute of Diagnostic and Interventional Neuroradiology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Lange, Claudia; 1Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Müller, Sebastian Johannes"],["dc.contributor.author","Khadhraoui, Eya"],["dc.contributor.author","Riedel, Christian Heiner"],["dc.contributor.author","Langer, Philip"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Timäus, Charles-Arnold"],["dc.contributor.author","Bouter, Caroline"],["dc.contributor.author","Ernst, Marielle"],["dc.contributor.author","Lange, Claudia"],["dc.date.accessioned","2022-12-01T08:31:32Z"],["dc.date.available","2022-12-01T08:31:32Z"],["dc.date.issued","2022"],["dc.date.updated","2022-11-11T13:12:44Z"],["dc.description.abstract","Background\r\n Dementia with Lewy bodies (DLB) is a type of dementia often diagnosed in older patients. Since its initial symptoms range from delirium to psychiatric and cognitive symptoms, the diagnosis is often delayed.\r\n \r\n \r\n Objectives\r\n In our study, we evaluated the magnetic resonance imaging (MRI) of patients suffering from DLB in correlation with their initial symptoms taking a new pragmatic approach entailing manual measurements in addition to an automated volumetric analysis of MRI.\r\n \r\n \r\n Methods\r\n \r\n A total of 63 patients with diagnosed DLB and valid 3D data sets were retrospectively and blinded evaluated. We assessed atrophy patterns (1) manually for the substantia innominata and (2)\r\n via\r\n FastSurfer for the most common supratentorial regions. Initial symptoms were categorized by (1) mild cognitive impairment (MCI), (2) psychiatric episodes, and (3) delirium.\r\n \r\n \r\n \r\n Results\r\n Manual metric MRI measurements revealed moderate, but significant substantia-innominata (SI) atrophy in patients with a psychiatric onset. FastSurfer analysis revealed no regional volumetric differences between groups.\r\n \r\n \r\n Conclusion\r\n The SI in patients with DLB and a psychiatric-onset is more atrophied than that in patients with initial MCI. Our results suggest potential differences in SI between DLB subtypes at the prodromal stage, which are useful when taking a differential-diagnostic approach. This finding should be confirmed in larger patient cohorts."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3389/fnagi.2022.815813"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118196"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1663-4365"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Metric magnetic resonance imaging analysis reveals pronounced substantia-innominata atrophy in dementia with Lewy bodies with a psychiatric onset"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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.journal","Frontiers in Psychiatry"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Bouter, Caroline"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Timäus, Charles"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Lange, Claudia"],["dc.date.accessioned","2021-04-14T08:23:48Z"],["dc.date.available","2021-04-14T08:23:48Z"],["dc.date.issued","2020"],["dc.description.abstract","Dementia with Lewy bodies (DLB) is the second most common form of dementia and is assumed to be often under- or misdiagnosed, especially in early stages. Here we present a complex case of probable DLB with major depression and alcohol and benzodiazepine dependence in which DLB was ruled out initially. This case highlights the challenging diagnostic workup of DLB patients. Core clinical features can be missing and indicative biomarkers can be negative, especially in early stages of the disease. Initially, Fluorodeoxyglucose positron emission tomography as well as neuropsychological assessment were suspicious for a possible DLB diagnosis in our patient while core clinical criteria were missing and the indicative biomarker 123I-FP-CIT SPECT was negative. Follow up was performed two years later and the patients showed several core and supportive clinical features of DLB and 123I-FP-CIT SPECT showed a pathological pattern. Extensive neuropsychological assessment in combination with PET imaging might provide crucial evidence for DLB even in early stages. If neuropsychology and PET imaging point to an early DLB diagnosis careful follow-up should be performed as core symptoms and indicative biomarkers might appear in later stages of the disease."],["dc.identifier.doi","10.3389/fpsyt.2020.00684"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17501"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81053"],["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.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Case Report: The Role of Neuropsychological Assessment and Imaging Biomarkers in the Early Diagnosis of Lewy Body Dementia in a Patient With Major Depression and Prolonged Alcohol and Benzodiazepine Dependence"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","121"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Alzheimer's Research & Therapy"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Shahpasand-Kroner, Hedieh"],["dc.contributor.author","Klafki, Hans-W."],["dc.contributor.author","Bauer, Chris"],["dc.contributor.author","Schuchhardt, Johannes"],["dc.contributor.author","Hüttenrauch, Melanie"],["dc.contributor.author","Stazi, Martina"],["dc.contributor.author","Bouter, Caroline"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Vogelgsang, Jonathan"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2019-07-09T11:49:37Z"],["dc.date.available","2019-07-09T11:49:37Z"],["dc.date.issued","2018"],["dc.description.abstract","Abstract Background The quantification of amyloid-beta (Aβ) peptides in blood plasma as potential biomarkers of Alzheimer’s disease (AD) is hampered by very low Aβ concentrations and the presence of matrix components that may interfere with the measurements. Methods We developed a two-step immunoassay for the simultaneous measurement of the relative levels of Aβ38, Aβ40 and Aβ42 in human EDTA plasma. The assay was employed for the study of 23 patients with dementia of the Alzheimer’s type (AD-D) and 17 patients with dementia due to other reasons (OD). We examined relationships with the clinical diagnosis, cerebral Aβ load as quantified by amyloid-positron emission tomography, apolipoprotein E genotype, Aβ levels and Tau protein in cerebrospinal fluid. Results Preconcentration of plasma Aβ peptides by immunoprecipitation substantially facilitated their immunological measurements. The Aβ42/Aβ40 and Aβ42/Aβ38 ratios were statistically significantly lower in the AD-D patients than in the OD group. The areas under the receiver operating characteristic curves reached 0.87 for the Aβ42/Aβ40 ratio and 0.80 for the Aβ42/Aβ38 ratio. Conclusions The measurement of plasma Aβ peptides with an immunological assay can be improved by preconcentration via immunoprecipitation with an antibody against the Aβ amino-terminus and elution of the captured peptides by heating in a mild detergent-containing buffer. Our findings support the Aβ42/Aβ40 ratio in blood plasma as a promising AD biomarker candidate which correlates significantly with the validated core biomarkers of AD. Further studies will be needed for technical advancement of the assay and validation of the biomarker findings."],["dc.identifier.doi","10.1186/s13195-018-0448-x"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15726"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59592"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","BioMed Central"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","A two-step immunoassay for the simultaneous assessment of Aβ38, Aβ40 and Aβ42 in human blood plasma supports the Aβ42/Aβ40 ratio as a promising biomarker candidate of Alzheimer’s disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Aging Neuroscience"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Lange, Claudia"],["dc.contributor.author","Timäus, Charles"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Bouter, Caroline"],["dc.date.accessioned","2021-08-12T07:45:44Z"],["dc.date.available","2021-08-12T07:45:44Z"],["dc.date.issued","2021"],["dc.description.abstract","Background (123)-I-2-ß-carbomethoxy-3ß-(4-iodophenyl)-N-(3-fluoropropyl) nortro- pane single photon emission computed tomography (123I-FP-CIT SPECT) was validated to distinguish Alzheimer’s dementia from dementia with Lewy Bodies (DLB) by European medical agencies. Little evidence exists that validates 123 I-FP-CIT SPECT as a supplementary method to diagnose probable DLB in a psychiatric cohort of patients with psychiatric symptomatology and suspected DLB. We aim to elucidate differences in the clinical phenotype of DLB between those patients with and those without a positive 123 I-FP-CIT SPECT indicating a nigrostriatal deficit. Methods To investigate this, we included 67 patients from the Department of Psychiatry and Psychotherapy at University Medical Center Göttingen (UMG) in our study who had undergone 123I-FP-CIT SPECT in the Department of Nuclear Medicine (UMG) by evaluating their patient files. Results 55% with a positive-123I-FP-CIT SPECT and probable DLB after the 123I-FP-CIT SPECT exhibited psychiatric features. The number of probable DLB patients in those exhibiting psychiatric symptoms was higher post-123I-FP-CIT SPECT than pre-123I-FP-CIT SPECT assessed cross-sectionally over a 6-year period ( p < 0.05). In addition, prodromal DLB and prodromal DLB patients with a psychiatric-phenotype yielded higher numbers post-123I-FP-CIT SPECT than pre-123I-FP-CIT SPECT ( p < 0.05). Furthermore, we discovered no phenotypical differences between those DLB patients with a positive and those with a negative 123I-FP-CIT SPECT. 123I-FP-CIT SPECT-positive DLB patients in our psychiatric cohort revealed a psychiatric onset more often (52%); DLB was less often characterized by an MCI onset (26%) ( p < 0.005). Conclusions Our findings support 123I-FP-CIT SPECT as an adjuvant tool for improving the diagnosis of probable DLB and prodromal DLB in a cohort of psychiatric patients with often concomitant psychiatric symptomatology. The psychiatric-onset is more frequent than an MCI-onset in DLB patients presenting nigrostriatal dysfunction, giving us an indication of the relevance of deep clinical phenotyping in memory clinics that includes the assessment of psychopathology."],["dc.description.abstract","Background (123)-I-2-ß-carbomethoxy-3ß-(4-iodophenyl)-N-(3-fluoropropyl) nortro- pane single photon emission computed tomography (123I-FP-CIT SPECT) was validated to distinguish Alzheimer’s dementia from dementia with Lewy Bodies (DLB) by European medical agencies. Little evidence exists that validates 123 I-FP-CIT SPECT as a supplementary method to diagnose probable DLB in a psychiatric cohort of patients with psychiatric symptomatology and suspected DLB. We aim to elucidate differences in the clinical phenotype of DLB between those patients with and those without a positive 123 I-FP-CIT SPECT indicating a nigrostriatal deficit. Methods To investigate this, we included 67 patients from the Department of Psychiatry and Psychotherapy at University Medical Center Göttingen (UMG) in our study who had undergone 123I-FP-CIT SPECT in the Department of Nuclear Medicine (UMG) by evaluating their patient files. Results 55% with a positive-123I-FP-CIT SPECT and probable DLB after the 123I-FP-CIT SPECT exhibited psychiatric features. The number of probable DLB patients in those exhibiting psychiatric symptoms was higher post-123I-FP-CIT SPECT than pre-123I-FP-CIT SPECT assessed cross-sectionally over a 6-year period ( p < 0.05). In addition, prodromal DLB and prodromal DLB patients with a psychiatric-phenotype yielded higher numbers post-123I-FP-CIT SPECT than pre-123I-FP-CIT SPECT ( p < 0.05). Furthermore, we discovered no phenotypical differences between those DLB patients with a positive and those with a negative 123I-FP-CIT SPECT. 123I-FP-CIT SPECT-positive DLB patients in our psychiatric cohort revealed a psychiatric onset more often (52%); DLB was less often characterized by an MCI onset (26%) ( p < 0.005). Conclusions Our findings support 123I-FP-CIT SPECT as an adjuvant tool for improving the diagnosis of probable DLB and prodromal DLB in a cohort of psychiatric patients with often concomitant psychiatric symptomatology. The psychiatric-onset is more frequent than an MCI-onset in DLB patients presenting nigrostriatal dysfunction, giving us an indication of the relevance of deep clinical phenotyping in memory clinics that includes the assessment of psychopathology."],["dc.description.sponsorship","Open-Access-Finanzierung durch die Universitätsmedizin Göttingen 2021"],["dc.identifier.doi","10.3389/fnagi.2021.672956"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88542"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.relation.eissn","1663-4365"],["dc.rights","CC BY 4.0"],["dc.title","Assessing Nigrostriatal Dopaminergic Pathways via 123I-FP-CIT SPECT in Dementia With Lewy Bodies in a Psychiatric Patient Cohort"],["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","127"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Alzheimer's Research & Therapy"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Klafki, Hans-W."],["dc.contributor.author","Vogelgsang, Jonathan"],["dc.contributor.author","Manuilova, Ekaterina"],["dc.contributor.author","Bauer, Chris"],["dc.contributor.author","Jethwa, Alexander"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Jahn-Brodmann, Anke"],["dc.contributor.author","Osterloh, Dirk"],["dc.contributor.author","Lachmann, Ingolf"],["dc.contributor.author","Breitling, Benedict"],["dc.contributor.author","Rauter, Carolin"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Bouter, Caroline"],["dc.contributor.author","Palme, Stefan"],["dc.contributor.author","Schuchhardt, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2022-09-12T07:56:44Z"],["dc.date.available","2022-09-12T07:56:44Z"],["dc.date.issued","2022-09-07"],["dc.date.updated","2022-09-11T03:10:27Z"],["dc.description.abstract","Abstract\r\n \r\n Background\r\n Measurements of the amyloid-β (Aβ) 42/40 ratio in blood plasma may support the early diagnosis of Alzheimer’s disease and aid in the selection of suitable participants in clinical trials. Here, we compared the diagnostic performance of fully automated prototype plasma Aβ42/40 assays with and without pre-analytical sample workup by immunoprecipitation.\r\n \r\n \r\n Methods\r\n A pre-selected clinical sample comprising 42 subjects with normal and 38 subjects with low cerebrospinal fluid (CSF) Aβ42/40 ratios was studied. The plasma Aβ42/40 ratios were determined with fully automated prototype Elecsys® immunoassays (Roche Diagnostics GmbH, Penzberg, Germany) by direct measurements in EDTA plasma or after pre-analytical Aβ immunoprecipitation. The diagnostic performance for the detection of abnormal CSF Aβ42/40 was analyzed by receiver operating characteristic (ROC) analysis. In an additional post hoc analysis, a biomarker-supported clinical diagnosis was used as a second endpoint.\r\n \r\n \r\n Results\r\n Pre-analytical immunoprecipitation resulted in a significant increase in the area under the ROC curve (AUC) from 0.73 to 0.88 (p = 0.01547) for identifying subjects with abnormal CSF Aβ42/40. A similar improvement in the diagnostic performance by pre-analytical immunoprecipitation was also observed when a biomarker-supported clinical diagnosis was used as a second endpoint (AUC increase from 0.77 to 0.92, p = 0.01576).\r\n \r\n \r\n Conclusions\r\n Our preliminary observations indicate that pre-analytical Aβ immunoprecipitation can improve the diagnostic performance of plasma Aβ assays for detecting brain amyloid pathology. The findings may aid in the further development of blood-based immunoassays for Alzheimer’s disease ultimately suitable for screening and routine use."],["dc.identifier.citation","Alzheimer's Research & Therapy. 2022 Sep 07;14(1):127"],["dc.identifier.doi","10.1186/s13195-022-01071-y"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114202"],["dc.language.iso","en"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)"],["dc.subject","Alzheimer’s disease"],["dc.subject","Biomarker assay"],["dc.subject","Plasma Amyloid-β 42/40"],["dc.subject","Immunoprecipitation"],["dc.subject","Pre-analytical sample workup"],["dc.title","Diagnostic performance of automated plasma amyloid-β assays combined with pre-analytical immunoprecipitation"],["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","114"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Neurology"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Khadhraoui, Eya"],["dc.contributor.author","Müller, Sebastian J."],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Riedel, Christian H."],["dc.contributor.author","Langer, Philip"],["dc.contributor.author","Timäeus, Charles"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Bouter, Caroline"],["dc.contributor.author","Lange, Claudia"],["dc.contributor.author","Ernst, Marielle"],["dc.date.accessioned","2022-04-01T10:01:59Z"],["dc.date.accessioned","2022-08-18T12:35:15Z"],["dc.date.available","2022-04-01T10:01:59Z"],["dc.date.available","2022-08-18T12:35:15Z"],["dc.date.issued","2022-03-24"],["dc.date.updated","2022-07-29T12:07:17Z"],["dc.description.abstract","Abstract\r\n \r\n Background\r\n Dementia with Lewy bodies (DLB) is the second most common dementia type in patients older than 65 years. Its atrophy patterns remain unknown. Its similarities to Parkinson's disease and differences from Alzheimer's disease are subjects of current research.\r\n \r\n \r\n Methods\r\n The aim of our study was (i) to form a group of patients with DLB (and a control group) and create a 3D MRI data set (ii) to volumetrically analyze the entire brain in these groups, (iii) to evaluate visual and manual metric measurements of the innominate substance for real-time diagnosis, and (iv) to compare our groups and results with the latest literature. We identified 102 patients with diagnosed DLB in our psychiatric and neurophysiological archives. After exclusion, 63 patients with valid 3D data sets remained. We compared them with a control group of 25 patients of equal age and sex distribution. We evaluated the atrophy patterns in both (1) manually and (2) via Fast Surfers segmentation and volumetric calculations. Subgroup analyses were done of the CSF data and quality of 3D T1 data sets.\r\n \r\n \r\n Results\r\n Concordant with the literature, we detected moderate, symmetric atrophy of the hippocampus, entorhinal cortex and amygdala, as well as asymmetric atrophy of the right parahippocampal gyrus in DLB. The caudate nucleus was unaffected in patients with DLB, while all the other measured territories were slightly too moderately atrophied. The area under the curve analysis of the left hippocampus volume ratio (< 3646mm3) revealed optimal 76% sensitivity and 100% specificity (followed by the right hippocampus and left amygdala). The substantia innominata’s visual score attained a 51% optimal sensitivity and 84% specificity, and the measured distance 51% optimal sensitivity and 68% specificity in differentiating DLB from our control group.\r\n \r\n \r\n Conclusions\r\n In contrast to other studies, we observed a caudate nucleus sparing atrophy of the whole brain in patients with DLB. As the caudate nucleus is known to be the last survivor in dopamine-uptake, this could be the result of an overstimulation or compensation mechanism deserving further investigation. Its relative hypertrophy compared to all other brain regions could enable an imaging based identification of patients with DLB via automated segmentation and combined volumetric analysis of the hippocampus and amygdala."],["dc.description.sponsorship","Georg-August-Universität Göttingen"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.citation","BMC Neurology. 2022 Mar 24;22(1):114"],["dc.identifier.doi","10.1186/s12883-022-02642-0"],["dc.identifier.pii","2642"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105794"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112938"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.publisher","BioMed Central"],["dc.relation.eissn","1471-2377"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject","Dementia with Lewy Bodies"],["dc.subject","MRI"],["dc.subject","Atrophy"],["dc.subject","Substantia innominate"],["dc.title","Manual and automated analysis of atrophy patterns in dementia with Lewy bodies on MRI"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","673"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Brain Sciences"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Lange, Claudia"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Hassoun, Lina"],["dc.contributor.author","Bouter, Caroline"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Schott, Björn Hendrik"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Fitzner, Dirk"],["dc.date.accessioned","2021-08-12T07:45:51Z"],["dc.date.available","2021-08-12T07:45:51Z"],["dc.date.issued","2021"],["dc.description.abstract","(1) Background: autoimmune encephalitis associated with neurexin-3α antibodies is a seldom reported disease entity often accompanied by a severe clinical neuropsychiatric syndrome. (2) Method: we report on the case of a 58-year-old man diagnosed with neurexin-3α-associated autoimmune encephalitis revealing cognitive decline and depression before the proof of neurexin-3α antibodies. He underwent neuropsychological testing, peripheral blood and cerebrospinal fluid analysis, neuroimaging and electroencephalography. (3) Results: our patient’s main clinical feature was amnestic cognitive decline in combination with depressive symptoms. CSF analysis showed elevated phosphorylated tau protein 181 and positive proof of serum neurexin-3α antibodies in a cell-based assay. An 18F-FDG-PET/CT of the brain initially showed bilateral cerebral hypometabolism prefrontal and parietal, which was absent in follow up. The brain MRI was unremarkable. EEG recordings showed frontotemporal slowing in the theta and delta range. (4) Conclusions: taken together, we assumed autoimmune encephalitis associated with serum neurexin-3α antibodies. To the best of our knowledge, we are the first to report on a predominantly mild clinical manifestation entailing amnestic mild cognitive impairment in addition to depression, thus broadening the clinical spectrum associated with neurexin-3α antibodies."],["dc.description.abstract","(1) Background: autoimmune encephalitis associated with neurexin-3α antibodies is a seldom reported disease entity often accompanied by a severe clinical neuropsychiatric syndrome. (2) Method: we report on the case of a 58-year-old man diagnosed with neurexin-3α-associated autoimmune encephalitis revealing cognitive decline and depression before the proof of neurexin-3α antibodies. He underwent neuropsychological testing, peripheral blood and cerebrospinal fluid analysis, neuroimaging and electroencephalography. (3) Results: our patient’s main clinical feature was amnestic cognitive decline in combination with depressive symptoms. CSF analysis showed elevated phosphorylated tau protein 181 and positive proof of serum neurexin-3α antibodies in a cell-based assay. An 18F-FDG-PET/CT of the brain initially showed bilateral cerebral hypometabolism prefrontal and parietal, which was absent in follow up. The brain MRI was unremarkable. EEG recordings showed frontotemporal slowing in the theta and delta range. (4) Conclusions: taken together, we assumed autoimmune encephalitis associated with serum neurexin-3α antibodies. To the best of our knowledge, we are the first to report on a predominantly mild clinical manifestation entailing amnestic mild cognitive impairment in addition to depression, thus broadening the clinical spectrum associated with neurexin-3α antibodies."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3390/brainsci11060673"],["dc.identifier.pii","brainsci11060673"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88559"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.relation.eissn","2076-3425"],["dc.rights","CC BY 4.0"],["dc.title","Mild Amnestic Cognitive Impairment and Depressive Symptoms in Autoimmune Encephalitis Associated with Serum Anti-Neurexin-3α Autoantibodies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]