Arnim, Christine A. F. von

[["dc.bibliographiccitation.artnumber","e0266906"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Yousefzadeh-Nowshahr, Elham"],["dc.contributor.author","Winter, Gordon"],["dc.contributor.author","Bohn, Peter"],["dc.contributor.author","Kneer, Katharina"],["dc.contributor.author","von Arnim, Christine A. F."],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Solbach, Christoph"],["dc.contributor.author","Anderl-Straub, Sarah"],["dc.contributor.author","Polivka, Dörte"],["dc.contributor.author","Fissler, Patrick"],["dc.contributor.authorgroup","for the Alzheimer’s Disease Neuroimaging Initiative"],["dc.contributor.editor","Su, Yi"],["dc.date.accessioned","2022-05-02T08:09:28Z"],["dc.date.available","2022-05-02T08:09:28Z"],["dc.date.issued","2022"],["dc.description.abstract","Purpose The recent developments of tau-positron emission tomography (tau-PET) enable in vivo assessment of neuropathological tau aggregates. Among the tau-specific tracers, the application of 11 C-pyridinyl-butadienyl-benzothiazole 3 ( 11 C-PBB3) in PET shows high sensitivity to Alzheimer disease (AD)-related tau deposition. The current study investigates the regional tau load in patients within the AD continuum, biomarker-negative individuals (BN) and patients with suspected non-AD pathophysiology (SNAP) using 11 C-PBB3-PET. Materials and methods A total of 23 memory clinic outpatients with recent decline of episodic memory were examined using 11 C-PBB3-PET. Pittsburg compound B ( 11 C-PIB) PET was available for 17, 18 F-flurodeoxyglucose ( 18 F-FDG) PET for 16, and cerebrospinal fluid (CSF) protein levels for 11 patients. CSF biomarkers were considered abnormal based on Aβ 42 (< 600 ng/L) and t-tau (> 450 ng/L). The PET biomarkers were classified as positive or negative using statistical parametric mapping (SPM) analysis and visual assessment. Using the amyloid/tau/neurodegeneration (A/T/N) scheme, patients were grouped as within the AD continuum, SNAP, and BN based on amyloid and neurodegeneration status. The 11 C-PBB3 load detected by PET was compared among the groups using both atlas-based and voxel-wise analyses. Results Seven patients were identified as within the AD continuum, 10 SNAP and 6 BN. In voxel-wise analysis, significantly higher 11 C-PBB3 binding was observed in the AD continuum group compared to the BN patients in the cingulate gyrus, tempo-parieto-occipital junction and frontal lobe. Compared to the SNAP group, patients within the AD continuum had a considerably increased 11 C-PBB3 uptake in the posterior cingulate cortex. There was no significant difference between SNAP and BN groups. The atlas-based analysis supported the outcome of the voxel-wise quantification analysis. Conclusion Our results suggest that 11 C-PBB3-PET can effectively analyze regional tau load and has the potential to differentiate patients in the AD continuum group from the BN and SNAP group."],["dc.description.abstract","Purpose The recent developments of tau-positron emission tomography (tau-PET) enable in vivo assessment of neuropathological tau aggregates. Among the tau-specific tracers, the application of 11 C-pyridinyl-butadienyl-benzothiazole 3 ( 11 C-PBB3) in PET shows high sensitivity to Alzheimer disease (AD)-related tau deposition. The current study investigates the regional tau load in patients within the AD continuum, biomarker-negative individuals (BN) and patients with suspected non-AD pathophysiology (SNAP) using 11 C-PBB3-PET. Materials and methods A total of 23 memory clinic outpatients with recent decline of episodic memory were examined using 11 C-PBB3-PET. Pittsburg compound B ( 11 C-PIB) PET was available for 17, 18 F-flurodeoxyglucose ( 18 F-FDG) PET for 16, and cerebrospinal fluid (CSF) protein levels for 11 patients. CSF biomarkers were considered abnormal based on Aβ 42 (< 600 ng/L) and t-tau (> 450 ng/L). The PET biomarkers were classified as positive or negative using statistical parametric mapping (SPM) analysis and visual assessment. Using the amyloid/tau/neurodegeneration (A/T/N) scheme, patients were grouped as within the AD continuum, SNAP, and BN based on amyloid and neurodegeneration status. The 11 C-PBB3 load detected by PET was compared among the groups using both atlas-based and voxel-wise analyses. Results Seven patients were identified as within the AD continuum, 10 SNAP and 6 BN. In voxel-wise analysis, significantly higher 11 C-PBB3 binding was observed in the AD continuum group compared to the BN patients in the cingulate gyrus, tempo-parieto-occipital junction and frontal lobe. Compared to the SNAP group, patients within the AD continuum had a considerably increased 11 C-PBB3 uptake in the posterior cingulate cortex. There was no significant difference between SNAP and BN groups. The atlas-based analysis supported the outcome of the voxel-wise quantification analysis. Conclusion Our results suggest that 11 C-PBB3-PET can effectively analyze regional tau load and has the potential to differentiate patients in the AD continuum group from the BN and SNAP group."],["dc.identifier.doi","10.1371/journal.pone.0266906"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107385"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-561"],["dc.relation.eissn","1932-6203"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Quantitative analysis of regional distribution of tau pathology with 11C-PBB3-PET in a clinical setting"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Alzheimer's Research & Therapy"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Halbgebauer, Steffen"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Riedel, Daniel"],["dc.contributor.author","Oeckl, Patrick"],["dc.contributor.author","Anderl-Straub, Sarah"],["dc.contributor.author","Lombardi, Jolina"],["dc.contributor.author","von Arnim, Christine A. F."],["dc.contributor.author","Nagl, Magdalena"],["dc.contributor.author","Giese, Armin"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2022-12-01T08:31:24Z"],["dc.date.available","2022-12-01T08:31:24Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract\n \n Background\n Visinin-like protein 1 (VILIP-1) belongs to the group of emerging biomarkers with the potential to support the early diagnosis of Alzheimer’s disease (AD). However, studies investigating the differential diagnostic potential in cerebrospinal fluid (CSF) are rare and are not available for blood.\n \n \n Methods\n We set up a novel, sensitive single molecule array (Simoa) assay for the detection of VILIP-1 in CSF and serum. In total, paired CSF and serum samples from 234 patients were investigated: 73 AD, 18 behavioral variant frontotemporal dementia (bvFTD), 26 parkinsonian syndromes, 20 amyotrophic lateral sclerosis (ALS), 22 Creutzfeldt-Jakob disease (CJD), and 75 non-neurodegenerative control (Con) patients. The differential diagnostic potential of CSF and serum VILIP-1 was assessed using the receiver operating characteristic curve analysis and findings were compared to core AD biomarkers.\n \n \n Results\n \n CSF and serum VILIP-1 levels correlated weakly (\n r\n =0.32 (CI: 0.20–0.43),\n p\n <0.0001). VILIP-1 concentrations in CSF and serum were elevated in AD compared to Con (\n p\n <0.0001 and\n p\n <0.01) and CJD (\n p\n <0.0001 for CSF and serum), and an increase in CSF was observed already in early AD stages (\n p\n <0.0001). In the discrimination of AD versus Con, we could demonstrate a strong diagnostic potential for CSF VILIP-1 alone (area under the curve (AUC): 0.87), CSF VILIP-1/CSF Abeta 1-42 (AUC: 0.98), and serum VILIP-1/CSF Abeta 1-42 ratio (AUC: 0.89).\n \n \n \n Conclusions\n We here report on the successful establishment of a novel Simoa assay for VILIP-1 and illustrate the potential of CSF and serum VILIP-1 in the differential diagnosis of AD with highest levels in CJD."],["dc.description.sponsorship","Intramural funding University of Ulm"],["dc.description.sponsorship","EU Joint Programme-Neurodegenerative Diseases networks Genfi-Prox"],["dc.description.sponsorship","German Federal Ministry of Education and Research"],["dc.description.sponsorship","EU (Moodmarker) program"],["dc.description.sponsorship","German Research Foundation/DFG"],["dc.description.sponsorship","Foundation of the state Baden-Württemberg"],["dc.description.sponsorship","Boehringer Ingelheim Ulm University BioCenter"],["dc.description.sponsorship","Thierry Latran Foundation"],["dc.description.sponsorship","Martin-Luther-Universität Halle-Wittenberg"],["dc.identifier.doi","10.1186/s13195-022-01122-4"],["dc.identifier.pii","1122"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118163"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.relation.eissn","1758-9193"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Visinin-like protein 1 levels in blood and CSF as emerging markers for Alzheimer’s and other neurodegenerative diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.volume","138"],["dc.contributor.author","Oeckl, Patrick"],["dc.contributor.author","Anderl-Straub, Sarah"],["dc.contributor.author","Diehl-Schmid, Janine"],["dc.contributor.author","von Arnim, Christine A. F."],["dc.contributor.author","Fassbender, Klaus"],["dc.contributor.author","Feneberg, Emily"],["dc.contributor.author","Fliessbach, Klaus"],["dc.contributor.author","Foerstl, Hans"],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Landwehrmeyer, Bernhard"],["dc.contributor.author","Lauer, Martin"],["dc.contributor.author","Levin, Johannes"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Prudlo, Johannes"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Schroeter, M."],["dc.contributor.author","Semler, Elisa"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Uttner, Ingo"],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Danek, A."],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T10:10:48Z"],["dc.date.available","2018-11-07T10:10:48Z"],["dc.date.issued","2016"],["dc.format.extent","355"],["dc.identifier.isi","000382568400345"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39931"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","10th International Conference on Frontotemporal Dementias"],["dc.relation.eventlocation","Munich, GERMANY"],["dc.relation.issn","1471-4159"],["dc.relation.issn","0022-3042"],["dc.title","Neurochemical markers in the differential diagnosis of primary progressive aphasias: Data from the German FTLD consortium"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","961"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","969"],["dc.bibliographiccitation.volume","88"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Semler, Elisa"],["dc.contributor.author","Anderl-Straub, Sarah"],["dc.contributor.author","Diehl-Schmid, Janine"],["dc.contributor.author","Schroeter, Matthias L."],["dc.contributor.author","Uttner, Ingo"],["dc.contributor.author","Foerstl, Hans"],["dc.contributor.author","Landwehrmeyer, Bernhard"],["dc.contributor.author","Kassubek, Jan"],["dc.contributor.author","Oeckl, Patrick"],["dc.contributor.author","Huppertz, Hans-Jürgen"],["dc.contributor.author","Fassbender, Klaus"],["dc.contributor.author","Fliessbach, Klaus"],["dc.contributor.author","Prudlo, Johannes"],["dc.contributor.author","Roßmeier, Carola"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Volk, Alexander E."],["dc.contributor.author","Lauer, Martin"],["dc.contributor.author","Danek, Adrian"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","von Arnim, Christine A. F."],["dc.date.accessioned","2020-12-10T18:41:44Z"],["dc.date.available","2020-12-10T18:41:44Z"],["dc.date.issued","2017"],["dc.description.abstract","Objective: To assess the utility of serum neurofilament for diagnosis and monitoring of primary progressive aphasia (PPA) variants. Methods: We investigated neurofilament light chain (NF-L) levels in blood of 99 patients with PPA (40 with nonfluent variant PPA [nfvPPA], 38 with semantic variant PPA [svPPA], 21 with logopenic variant PPA [lvPPA]) and compared diagnostic performance with that reached by CSF NF-L, phosphorylated neurofilament heavy chain (pNF-H), b-amyloid (Ab(1)-42), tau, and phosphorylated tau. The longitudinal change of blood NF-L levels was measured and analyzed for correlation with functional decline and brain atrophy. Results: Serum NF-L is increased in PPA compared to controls and discriminates between nfvPPA/svPPA and lvPPA with 81% sensitivity and 67% specificity (cutoff 31 pg/mL). CSF NF-L, pNF-H, tau, phosphorylated tau, and Ab1-42 achieved similar performance, and pNF-H was the only marker for discrimination of nfvPPA from svPPA/lvPPA. In most patients with nfvPPA and svPPA, but not lvPPA, serum NF-L increased within follow-up. The increase correlated with functional decline and progression of atrophy of the left frontal lobe of all patients with PPAs and the right middle frontal gyrus of patients with nfvPPA and svPPA. Conclusions: Blood level of NF-L can aid the differential diagnosis of PPA variants, especially in combination with CSF pNF-H. Because serum NF-L correlates with functional decline and atrophy in the disease course, it qualifies as an objective disease status marker. Extended follow-up studies with cases of known neuropathology are imperative."],["dc.identifier.doi","10.1212/WNL.0000000000003688"],["dc.identifier.eissn","1526-632X"],["dc.identifier.isi","000397343300012"],["dc.identifier.issn","0028-3878"],["dc.identifier.pmid","28179468"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77660"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Neurofilament as a blood marker for diagnosis and monitoring of primary progressive aphasias"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","jnnp-2021-328646"],["dc.bibliographiccitation.journal","Journal of Neurology, Neurosurgery & Psychiatry"],["dc.contributor.author","Halbgebauer, Steffen"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Hengge, Sophie"],["dc.contributor.author","Oeckl, Patrick"],["dc.contributor.author","Abu Rumeileh, Samir"],["dc.contributor.author","Anderl-Straub, Sarah"],["dc.contributor.author","Lombardi, Jolina"],["dc.contributor.author","Von Arnim, Christine A F"],["dc.contributor.author","Giese, Armin"],["dc.contributor.author","Ludolph, Albert C"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2022-09-01T09:50:49Z"],["dc.date.available","2022-09-01T09:50:49Z"],["dc.date.issued","2022"],["dc.description.abstract","Background\r\n Synaptosomal-associated protein 25 (SNAP-25) in cerebrospinal fluid (CSF) is an emerging synaptic biomarker for the early diagnosis of Alzheimer’s disease (AD). However, comprehensive studies investigating the marker in Creutzfeldt-Jakob disease (CJD) and in the differential diagnosis of neurodegenerative diseases are still lacking.\r\n \r\n \r\n Methods\r\n We developed a novel, sensitive ELISA for the measurement of SNAP-25 in CSF. In total, we analysed 316 patients from 6 diagnostic groups comprising patients with AD (n=96), CJD (n=55), Parkinson’s disease spectrum (n=41), frontotemporal lobar degeneration (n=25) and amyotrophic lateral sclerosis (n=24) and non-neurodegenerative control patients (n=75). Using receiver operating characteristic curve analysis, we analysed the differential diagnostic potential and compared the results with core AD biomarkers.\r\n \r\n \r\n Results\r\n SNAP-25 CSF concentrations were elevated in AD and CJD (p<0.0001) but not in the other neurodegenerative diseases. Increased levels were observed already at early AD and CJD stages (p<0.0001). In CJD, SNAP-25 levels correlated negatively with survival time (r=−0.33 (95% CI −0.57 to −0.04, p=0.02). For the discrimination of AD from all other diseases except CJD, we observed a good diagnostic performance for CSF SNAP-25 (area under the curve (AUC) 0.85) which was further improved by applying the ratio with CSF amyloid-β 1–42 (AUC 0.95). For CJD, we could demonstrate a strong differential diagnostic potential against all other groups including AD (AUC 0.97).\r\n \r\n \r\n Conclusion\r\n Using the novel established CSF SNAP-25 ELISA, we here demonstrate the applicability of SNAP-25 as an early synaptic biomarker for both AD and CJD with a possible prognostic value in patients with CJD."],["dc.description.sponsorship","Thierry Latran Foundation"],["dc.description.sponsorship","Boehringer Ingelheim Ulm University BioCenter"],["dc.description.sponsorship","EU Moodmarker programme"],["dc.description.sponsorship","FederalMinistry of Education and Research"],["dc.description.sponsorship","German Research Foundation/DFG"],["dc.description.sponsorship","The foundation of the state Baden-Württemberg"],["dc.description.sponsorship","EU Joint Programme-Neurodegenerative Diseases"],["dc.identifier.doi","10.1136/jnnp-2021-328646"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/113813"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-597"],["dc.relation.eissn","1468-330X"],["dc.relation.issn","0022-3050"],["dc.title","CSF levels of SNAP-25 are increased early in Creutzfeldt-Jakob and Alzheimer’s disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]