Göbel, Stefan

[["dc.bibliographiccitation.firstpage","1259"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Diagnostics"],["dc.bibliographiccitation.volume","12"],["dc.contributor.affiliation","Emdina, Anna; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Hermann, Peter; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Varges, Daniela; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Nuhn, Sabine; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Goebel, Stefan; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Bunck, Timothy; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Maass, Fabian; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Schmitz, Matthias; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Llorens, Franc; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Kruse, Niels; 4Department of Neuropathology, University Medical Centre Göttingen, 37075 Göttingen, Germany; n.kruse@med.uni-goettingen.de"],["dc.contributor.affiliation","Lingor, Paul; 5Department of Neurology, Klinikum Rechts der Isar, Technical University of Munich, 80333 Munich, Germany; paul.lingor@tum.de"],["dc.contributor.affiliation","Mollenhauer, Brit; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.affiliation","Zerr, Inga; 1Department of Neurology, University Medical Center Göttingen, 37075 Göttingen, Germany; anna.emdina@stud.uni-goettingen.de (A.E.); d.varges@med.uni-goettingen.de (D.V.); sabine.nuhn@med.uni-goettingen.de (S.N.); stefan.goebel@med.uni-goettingen.de (S.G.); timothy.bunck@med.uni-goettingen.de (T.B.); fabian.maass@med.uni-goettingen.de (F.M.); matthias.schmitz@med.uni-goettingen.de (M.S.); franc.llorens@gmail.com (F.L.); brit.mollenhauer@med.uni-goettingen.de (B.M.); ingazerr@med.uni-goettingen.de (I.Z.)"],["dc.contributor.author","Emdina, Anna"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Varges, Daniela"],["dc.contributor.author","Nuhn, Sabine"],["dc.contributor.author","Goebel, Stefan"],["dc.contributor.author","Bunck, Timothy"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Mollenhauer, Brit"],["dc.date.accessioned","2022-06-01T09:39:57Z"],["dc.date.available","2022-06-01T09:39:57Z"],["dc.date.issued","2022"],["dc.date.updated","2022-06-05T20:43:26Z"],["dc.description.abstract","Biomarkers are increasingly recognized as tools in the diagnosis and prognosis of neurodegenerative diseases. No fluid biomarker for Parkinson’s disease (PD) has been established to date, but α-synuclein, a major component of Lewy bodies in PD and dementia with Lewy bodies (DLB), has become a promising candidate. Here, we investigated CSF α-synuclein in patients with PD (n = 28), PDD (n = 8), and DLB (n = 5), applying an electrochemiluminescence immunoassay. Median values were non-significantly (p = 0.430) higher in patients with PDD and DLB (287 pg/mL) than in PD (236 pg/mL). A group of n = 36 primarily non-demented patients with PD and PDD was clinically followed for up to two years. A higher baseline α-synuclein was associated with increases in Hoehn and Yahr classifications (p = 0.019) and Beck Depression Inventory scores (p < 0.001) as well as worse performance in Trail Making Test A (p = 0.017), Trail Making Test B (p = 0.043), and the Boston Naming Test (p = 0.002) at follow-up. Surprisingly, higher levels were associated with a better performance in semantic verbal fluency tests (p = 0.046). In summary, CSF α-synuclein may be a potential prognostic marker for disease progression, affective symptoms, and executive cognitive function in PD. Larger-scaled studies have to validate these findings and the discordant results for single cognitive tests in this exploratory investigation."],["dc.identifier.doi","10.3390/diagnostics12051259"],["dc.identifier.pii","diagnostics12051259"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108601"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.eissn","2075-4418"],["dc.title","Baseline Cerebrospinal Fluid α-Synuclein in Parkinson’s Disease Is Associated with Disease Progression and Cognitive Decline"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Villar-Piqué, Anna"],["dc.contributor.author","Diaz-Lucena, Daniela"],["dc.contributor.author","Nägga, Katarina"],["dc.contributor.author","Hansson, Oskar"],["dc.contributor.author","Santana, Isabel"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Schmidt, Christian"],["dc.contributor.author","Varges, Daniela"],["dc.contributor.author","Goebel, Stefan"],["dc.contributor.author","Dumurgier, Julien"],["dc.contributor.author","Zetterberg, Henrik"],["dc.contributor.author","Blennow, Kaj"],["dc.contributor.author","Paquet, Claire"],["dc.contributor.author","Baldeiras, Inês"],["dc.contributor.author","Ferrer, Isidro"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2021-04-14T08:27:37Z"],["dc.date.available","2021-04-14T08:27:37Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1038/s41467-020-14373-2"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17201"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82349"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2041-1723"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Cerebrospinal fluid lipocalin 2 as a novel biomarker for the differential diagnosis of vascular dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1841"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","European Journal of Neurology"],["dc.bibliographiccitation.lastpage","1846"],["dc.bibliographiccitation.volume","29"],["dc.contributor.affiliation","Canaslan, Sezgi; 1\r\nDepartment of Neurology\r\nNational Reference Center for CJD Surveillance\r\nGöttingen University Medical Center\r\nGöttingen Germany"],["dc.contributor.affiliation","Villar‐Piqué, Anna; 2\r\nBellvitge Biomedical Research Institute\r\nHospitalet de Llobregat Spain"],["dc.contributor.affiliation","Bunck, Timothy; 1\r\nDepartment of Neurology\r\nNational Reference Center for CJD Surveillance\r\nGöttingen University Medical Center\r\nGöttingen Germany"],["dc.contributor.affiliation","Goebel, Stefan; 1\r\nDepartment of Neurology\r\nNational Reference Center for CJD Surveillance\r\nGöttingen University Medical Center\r\nGöttingen Germany"],["dc.contributor.affiliation","Llorens, Franc; 1\r\nDepartment of Neurology\r\nNational Reference Center for CJD Surveillance\r\nGöttingen University Medical Center\r\nGöttingen Germany"],["dc.contributor.affiliation","Schmitz, Matthias; 1\r\nDepartment of Neurology\r\nNational Reference Center for CJD Surveillance\r\nGöttingen University Medical Center\r\nGöttingen Germany"],["dc.contributor.affiliation","Zerr, Inga; 1\r\nDepartment of Neurology\r\nNational Reference Center for CJD Surveillance\r\nGöttingen University Medical Center\r\nGöttingen Germany"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Canaslan, Sezgi"],["dc.contributor.author","Villar‐Piqué, Anna"],["dc.contributor.author","Bunck, Timothy"],["dc.contributor.author","Goebel, Stefan"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2022-04-01T10:03:27Z"],["dc.date.available","2022-04-01T10:03:27Z"],["dc.date.issued","2022"],["dc.date.updated","2022-06-14T22:22:24Z"],["dc.description.abstract","Abstract Background and purpose Fatal familial insomnia is a rare hereditary prion disease associated with the D178N‐129M PRNP mutation. Early diagnosis is difficult, because the clinical syndrome may overlap with affective disorders. In addition, most known cerebrospinal fluid biomarkers for prion diseases and magnetic resonance imaging do not show a good diagnostic accuracy for fatal familial insomnia. In this context, data on plasma biomarkers are scarce. Methods We analyzed levels of neurofilament light chain, glial fibrillary acidic protein, chitinase‐3‐like protein 1, calcium‐binding protein B, and total tau protein in six serial plasma samples from a patient with fatal familial insomnia. Subsequently, plasma neurofilament light chain was analyzed in n = 25 patients and n = 19 controls. The diagnostic accuracy and associations with disease stage and duration were explored. Results Among all biomarker candidates in the case study, only neurofilament light chain levels showed a constant evolution and increased over time. They discriminated fatal familial insomnia from controls with an area under the curve of 0.992 (95% confidence interval [CI] = 0.974–1) in the case–control study. Higher concentrations were associated with methionine homozygosity at codon 129 PRNP (p = 0.006), shorter total disease duration (rho = −0.467, p = 0.019, 95% CI = −0.790 to −0.015), and shorter time from sampling to death (rho = −0.467, p = 0.019, 95% CI = −0.773 to −0.019). Conclusions Plasma neurofilament light chain may be a valuable minimally invasive diagnostic biomarker for fatal familial insomnia after clinical onset. Most important, stage‐related increase and association with disease duration indicate potential as a prognostic marker and as a surrogate marker in clinical trials."],["dc.description.abstract","We investigated plasma biomarkers during preclinical and clinical phase in a patient with fatal familial insomnia (FFI) and identified a stage‐related increase of neurofilament light chain (NfL) from disease onset to late clinical stage. In a retrospective analysis, we observed high discriminatory value of plasma NfL in 25 FFI patients versus 19 control patients (area under the curve = 0.992). In FFI, higher NfL concentrations were significantly associated with shorter overall disease duration and shorter time from sampling to death. image"],["dc.description.sponsorship","CJD Foundation"],["dc.description.sponsorship","Alzheimer Forschung Initiative http://dx.doi.org/10.13039/100010146"],["dc.description.sponsorship","Robert‐Koch‐Institute"],["dc.identifier.doi","10.1111/ene.15302"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/106170"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","1468-1331"],["dc.relation.issn","1351-5101"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes."],["dc.title","Plasma neurofilament light chain as a biomarker for fatal familial insomnia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","145"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Villar-Piqué, Anna"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Goebel, Stefan"],["dc.contributor.author","Bunck, Timothy"],["dc.contributor.author","Varges, Daniela"],["dc.contributor.author","Ferrer, Isidre"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2019-07-16T09:49:35Z"],["dc.date.available","2019-07-16T09:49:35Z"],["dc.date.issued","2019"],["dc.description.abstract","Increased plasma YKL-40 has been reported in Alzheimer's disease (AD), but its levels in other neurodegenerative diseases are unknown. Here, we aimed to investigate plasma YKL-40 in the spectrum of neurodegenerative dementias."],["dc.identifier.doi","10.1186/s12974-019-1531-3"],["dc.identifier.pmid","31299989"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16273"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61559"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1742-2094"],["dc.relation.issn","1742-2094"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Plasma YKL-40 in the spectrum of neurodegenerative dementia"],["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"]]