Arnim, Christine A. F. von

[["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.firstpage","68"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neurology, Neurosurgery & Psychiatry"],["dc.bibliographiccitation.lastpage","74"],["dc.bibliographiccitation.volume","93"],["dc.contributor.author","Halbgebauer, Steffen"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Verde, Federico"],["dc.contributor.author","Weishaupt, Jochen"],["dc.contributor.author","Oeckl, Patrick"],["dc.contributor.author","von Arnim, Christine"],["dc.contributor.author","Dorst, Johannes"],["dc.contributor.author","Feneberg, Emily"],["dc.contributor.author","Mayer, Benjamin"],["dc.contributor.author","Rosenbohm, Angela"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2022-01-11T14:06:04Z"],["dc.date.available","2022-01-11T14:06:04Z"],["dc.date.issued","2021"],["dc.description.abstract","Objective Elevated levels of neurofilament light (NfL) and heavy (NfH) chain in amyotrophic lateral sclerosis (ALS) cerebrospinal fluid (CSF) and serum reflect neuro-axonal degeneration and are used as diagnostic biomarkers. However, studies comparing the differential diagnostic potential for ALS of all four parameters are missing. Here, we measured serum NfL/NfH and CSF NfL/NfH in a large cohort of ALS and other neurological disorders and analysed the differential diagnostic potential. Methods In total CSF and serum of 294 patients were analysed. The diagnostic groups comprised: ALS (n=75), frontotemporal lobar degeneration (FTLD) (n=33), Alzheimer’s disease (n=20), Parkinson’s disease (dementia) (n=18), Creutzfeldt-Jakob disease (n=11), non-neurodegenerative controls (n=77) (Con) and 60 patients who were seen under the direct differential diagnosis of a patient with ALS (Con.DD). Results CSF and serum NfL and NfH showed significantly increased levels in ALS (p<0.0001) compared with Con and Con.DD. The difference between ALS and FTLD was markedly stronger for NfH than for NfL. CSF and serum NfL demonstrated a stronger correlation (r=0.84 (95% CI 0.80 to 0.87), p<0.001) than CSF and serum NfH (r=0.68 (95% CI 0.61 to 0.75), p<0.0001). Comparing ALS and Con.DD, receiver operating characteristic analysis revealed the best area under the curve (AUC) value for CSF NfL (AUC=0.94, 95% CI 0.91 to 0.98), followed by CSF NfH (0.93, 95% CI 0.88 to 0.98), serum NfL (0.93, 95% CI 0.89 to 0.97) and serum NfH (0.88, 95% CI 0.82 to 0.94). Conclusion Our results demonstrate that CSF NfL and NfH as well as serum NfL are equally suited for the differential diagnosis of ALS, whereas serum NfH appears to be slightly less potent."],["dc.description.abstract","Objective Elevated levels of neurofilament light (NfL) and heavy (NfH) chain in amyotrophic lateral sclerosis (ALS) cerebrospinal fluid (CSF) and serum reflect neuro-axonal degeneration and are used as diagnostic biomarkers. However, studies comparing the differential diagnostic potential for ALS of all four parameters are missing. Here, we measured serum NfL/NfH and CSF NfL/NfH in a large cohort of ALS and other neurological disorders and analysed the differential diagnostic potential. Methods In total CSF and serum of 294 patients were analysed. The diagnostic groups comprised: ALS (n=75), frontotemporal lobar degeneration (FTLD) (n=33), Alzheimer’s disease (n=20), Parkinson’s disease (dementia) (n=18), Creutzfeldt-Jakob disease (n=11), non-neurodegenerative controls (n=77) (Con) and 60 patients who were seen under the direct differential diagnosis of a patient with ALS (Con.DD). Results CSF and serum NfL and NfH showed significantly increased levels in ALS (p<0.0001) compared with Con and Con.DD. The difference between ALS and FTLD was markedly stronger for NfH than for NfL. CSF and serum NfL demonstrated a stronger correlation (r=0.84 (95% CI 0.80 to 0.87), p<0.001) than CSF and serum NfH (r=0.68 (95% CI 0.61 to 0.75), p<0.0001). Comparing ALS and Con.DD, receiver operating characteristic analysis revealed the best area under the curve (AUC) value for CSF NfL (AUC=0.94, 95% CI 0.91 to 0.98), followed by CSF NfH (0.93, 95% CI 0.88 to 0.98), serum NfL (0.93, 95% CI 0.89 to 0.97) and serum NfH (0.88, 95% CI 0.82 to 0.94). Conclusion Our results demonstrate that CSF NfL and NfH as well as serum NfL are equally suited for the differential diagnosis of ALS, whereas serum NfH appears to be slightly less potent."],["dc.identifier.doi","10.1136/jnnp-2021-327129"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97819"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-507"],["dc.relation.eissn","1468-330X"],["dc.relation.issn","0022-3050"],["dc.title","Comparison of CSF and serum neurofilament light and heavy chain as differential diagnostic biomarkers for ALS"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e48783"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Jesse, Sarah"],["dc.contributor.author","Lehnert, Stefan"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Parnetti, Lucilla"],["dc.contributor.author","Soininen, Hilkka"],["dc.contributor.author","Herukka, Sanna-Kaisa"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Tawfik, Saskia"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","von Arnim, Christine A. F."],["dc.contributor.author","Neumann, Manuela"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Kulaksiz, Hasan"],["dc.contributor.author","Lenter, Martin"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Ferger, Boris"],["dc.contributor.author","Hengerer, Bastian"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2019-07-09T11:53:59Z"],["dc.date.available","2019-07-09T11:53:59Z"],["dc.date.issued","2012-11-08"],["dc.description.abstract","The prevalence of Parkinson’s disease (PD) increases with age. Up to 50% of PD show cognitive decline in terms of a mild cognitive impairment already in early stages that predict the development of dementia, which can occur in up to 80% of PD patients over the long term, called Parkinson’s disease dementia (PDD). So far, diagnosis of PD/PDD is made according to clinical and neuropsychological examinations while laboratory data is only used for exclusion of other diseases. The aim of this study was the identification of possible biomarkers in cerebrospinal fluid (CSF) of PD, PDD and controls (CON) which predict the development of dementia in PD. For this, a proteomic approach optimized for CSF was performed using 18 clinically well characterized patients in a first step with subsequent validation using 84 patients. Here, we detected differentially sialylated isoforms of Serpin A1 as marker for differentiation of PD versus PDD in CSF. Performing 2Dimmunoblots, all PDD patients could be identified correctly (sensitivity 100%). Ten out of 24 PD patients showed Serpin A1 isoforms in a similar pattern like PDD, indicating a specificity of 58% for the test-procedure. In control samples, no additional isoform was detected. On the basis of these results, we conclude that differentially sialylated products of Serpin A1 are an interesting biomarker to indicate the development of a dementia during the course of PD."],["dc.format.extent","10"],["dc.identifier.doi","10.1371/journal.pone.0048783"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8304"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60545"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Differential Sialylation of Serpin A1 in the Early Diagnosis of Parkinson’s Disease Dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["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"]]