Zerr, Inga

[["dc.bibliographiccitation.artnumber","86"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Alzheimer's Research & Therapy"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Villar-Piqué, Anna"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Varges, Daniela"],["dc.contributor.author","Ferrer, Isidre"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Zetterberg, Henrik"],["dc.contributor.author","Blennow, Kaj"],["dc.contributor.author","Llorens, Franc"],["dc.date.accessioned","2021-06-01T09:42:16Z"],["dc.date.accessioned","2022-08-18T12:38:53Z"],["dc.date.available","2021-06-01T09:42:16Z"],["dc.date.available","2022-08-18T12:38:53Z"],["dc.date.issued","2021-04-21"],["dc.date.updated","2022-07-29T12:17:47Z"],["dc.description.abstract","Abstract\r\n \r\n Background\r\n Blood neurofilament light (Nfl) and total-tau (t-tau) have been described to be increased in several neurological conditions, including prion diseases and other neurodegenerative dementias. Here, we aim to determine the accuracy of plasma Nfl and t-tau in the differential diagnosis of neurodegenerative dementias and their potential value as prognostic markers of disease severity.\r\n \r\n \r\n Methods\r\n Plasma Nfl and t-tau were measured in healthy controls (HC, n = 70), non-neurodegenerative neurological disease with (NND-Dem, n = 17) and without dementia syndrome (NND, n = 26), Alzheimer’s disease (AD, n = 44), Creutzfeldt-Jakob disease (CJD, n = 83), dementia with Lewy bodies/Parkinson’s disease with dementia (DLB/PDD, n = 35), frontotemporal dementia (FTD, n = 12), and vascular dementia (VaD, n = 22). Biomarker diagnostic accuracies and cutoff points for the diagnosis of CJD were calculated, and associations between Nfl and t-tau concentrations with other fluid biomarkers, demographic, genetic, and clinical data in CJD cases were assessed. Additionally, the value of Nfl and t-tau predicting disease survival in CJD was evaluated.\r\n \r\n \r\n Results\r\n Among diagnostic groups, highest plasma Nfl and t-tau concentrations were detected in CJD (fold changes of 38 and 18, respectively, compared to HC). Elevated t-tau was able to differentiate CJD from all other groups, whereas elevated Nfl concentrations were also detected in NND-Dem, AD, DLB/PDD, FTD, and VaD compared to HC. Both biomarkers discriminated CJD from non-CJD dementias with an AUC of 0.93. In CJD, plasma t-tau, but not Nfl, was associated with PRNP codon 129 genotype and CJD subtype. Positive correlations were observed between plasma Nfl and t-tau concentrations, as well as between plasma and CSF concentrations of both biomarkers (p < 0.001). Nfl was increased in rapidly progressive AD (rpAD) compared to slow progressive AD (spAD) and associated to Mini-Mental State Examination results. However, Nfl displayed higher accuracy than t-tau discriminating CJD from rpAD and spAD. Finally, plasma t-tau, but not plasma Nfl, was significantly associated with disease duration, offering a moderate survival prediction capacity.\r\n \r\n \r\n Conclusions\r\n Plasma Nfl and t-tau are useful complementary biomarkers for the differential diagnosis of CJD. Additionally, plasma t-tau emerges as a potential prognostic marker of disease duration."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.citation","Alzheimer's Research & Therapy. 2021 Apr 21;13(1):86"],["dc.identifier.doi","10.1186/s13195-021-00815-6"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17765"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85196"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112965"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","BioMed Central"],["dc.relation.eissn","1758-9193"],["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"],["dc.subject","Creutzfeldt-Jakob disease"],["dc.subject","Biomarkers"],["dc.subject","Plasma"],["dc.subject","Neurofilament light"],["dc.subject","Tau"],["dc.subject","Diagnosis"],["dc.subject","Disease progression"],["dc.title","Diagnostic and prognostic value of plasma neurofilament light and total-tau in sporadic Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","9"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Alzheimer's Research & Therapy"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Villar-Piqué, Anna"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Schmidt, Christian"],["dc.contributor.author","Varges, Daniela"],["dc.contributor.author","Goebel, Stefan"],["dc.contributor.author","Bunck, Timothy"],["dc.contributor.author","Lindemann, Hanna"],["dc.contributor.author","Bogner, Carla"],["dc.contributor.author","Santana, Isabel"],["dc.contributor.author","Baldeiras, Inês"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Llorens, Franc"],["dc.date.accessioned","2022-02-01T10:31:33Z"],["dc.date.accessioned","2022-08-18T12:39:24Z"],["dc.date.available","2022-02-01T10:31:33Z"],["dc.date.available","2022-08-18T12:39:24Z"],["dc.date.issued","2022-01-13"],["dc.date.updated","2022-07-29T12:17:51Z"],["dc.description.abstract","Background Lipocalin-2 is a glycoprotein that is involved in various physiological and pathophysiological processes. In the brain, it is expressed in response to vascular and other brain injury, as well as in Alzheimer’s disease in reactive microglia and astrocytes. Plasma Lipocalin-2 has been proposed as a biomarker for Alzheimer’s disease but available data is scarce and inconsistent. Thus, we evaluated plasma Lipocalin-2 in the context of Alzheimer’s disease, differential diagnoses, other biomarkers, and clinical data. Methods For this two-center case-control study, we analyzed Lipocalin-2 concentrations in plasma samples from a cohort of n  = 407 individuals. The diagnostic groups comprised Alzheimer’s disease ( n  = 74), vascular dementia ( n  = 28), other important differential diagnoses ( n  = 221), and healthy controls ( n  = 84). Main results were validated in an independent cohort with patients with Alzheimer’s disease ( n  = 19), mild cognitive impairment ( n  = 27), and healthy individuals ( n  = 28). Results Plasma Lipocalin-2 was significantly lower in Alzheimer’s disease compared to healthy controls ( p  < 0.001) and all other groups ( p  < 0.01) except for mixed dementia (vascular and Alzheimer’s pathologic changes). Areas under the curve from receiver operation characteristics for the discrimination of Alzheimer’s disease and healthy controls were 0.783 (95%CI: 0.712–0.855) in the study cohort and 0.766 (95%CI: 0.627–0.905) in the validation cohort. The area under the curve for Alzheimer’s disease versus vascular dementia was 0.778 (95%CI: 0.667–0.890) in the study cohort. In Alzheimer’s disease patients, plasma Lipocalin2 did not show significant correlation with cerebrospinal fluid biomarkers of neurodegeneration and AD-related pathology (total-tau, phosphorylated tau protein, and beta-amyloid 1-42), cognitive status (Mini Mental Status Examination scores), APOE genotype, or presence of white matter hyperintensities. Interestingly, Lipocalin 2 was lower in patients with rapid disease course compared to patients with non-rapidly progressive Alzheimer’s disease ( p  = 0.013). Conclusions Plasma Lipocalin-2 has potential as a diagnostic biomarker for Alzheimer’s disease and seems to be independent from currently employed biomarkers."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.citation","Alzheimer's Research & Therapy. 2022 Jan 13;14(1):9"],["dc.identifier.doi","10.1186/s13195-021-00955-9"],["dc.identifier.pii","955"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/98886"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112969"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-517"],["dc.publisher","BioMed Central"],["dc.relation.eissn","1758-9193"],["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"],["dc.subject","Alzheimer’s disease"],["dc.subject","Biomarker"],["dc.subject","Plasma"],["dc.subject","Lipocalin 2"],["dc.subject","Neutrophil gelatinase-associated Lipocalin"],["dc.title","Plasma Lipocalin 2 in Alzheimer’s disease: potential utility in the differential diagnosis and relationship with other biomarkers"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]