Hermann, Peter

[["dc.bibliographiccitation.firstpage","6298"],["dc.bibliographiccitation.issue","17"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","21"],["dc.contributor.affiliation","Podlesniy, Petar; \t\t \r\n\t\t Neurobiology Unit, Institut d’Investigacions Biomèdiques de Barcelona (CSIC), 08036 Barcelona, Spain, ppodlesniy@gmail.com\t\t \r\n\t\t Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), 08036 Barcelona, Spain, ppodlesniy@gmail.com"],["dc.contributor.affiliation","Llorens, Franc; \t\t \r\n\t\t Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), 08036 Barcelona, Spain, franc.llorens@gmail.com\t\t \r\n\t\t Bellvitge Biomedical Research Institute (IBIDELL), 08908 L’Hospitalet de Llobregat, Spain, franc.llorens@gmail.com\t\t \r\n\t\t Department of Neurology, Clinical Dementia Center, University Medical School, Georg-August University, 37075 Göttingen, Germany, franc.llorens@gmail.com"],["dc.contributor.affiliation","Puigròs, Margalida; \t\t \r\n\t\t Neurobiology Unit, Institut d’Investigacions Biomèdiques de Barcelona (CSIC), 08036 Barcelona, Spain, puigrosserra.m@gmail.com\t\t \r\n\t\t Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), 08036 Barcelona, Spain, puigrosserra.m@gmail.com"],["dc.contributor.affiliation","Serra, Nuria; \t\t \r\n\t\t Neurobiology Unit, Institut d’Investigacions Biomèdiques de Barcelona (CSIC), 08036 Barcelona, Spain, serranuri@gmail.com\t\t \r\n\t\t Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), 08036 Barcelona, Spain, serranuri@gmail.com"],["dc.contributor.affiliation","Sepúlveda-Falla, Diego; \t\t \r\n\t\t Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany, d.sepulveda-falla@uke.uni-hamburg.de"],["dc.contributor.affiliation","Schmidt, Christian; \t\t \r\n\t\t Department of Neurology, Clinical Dementia Center, University Medical School, Georg-August University, 37075 Göttingen, Germany, Christian.Schmidt@medizin.uni-goettingen.de\t\t \r\n\t\t German Center for Neurodegenerative Diseases (DZNE), 37075 Göttingen, Germany, Christian.Schmidt@medizin.uni-goettingen.de"],["dc.contributor.affiliation","Hermann, Peter; \t\t \r\n\t\t Department of Neurology, Clinical Dementia Center, University Medical School, Georg-August University, 37075 Göttingen, Germany, peter.hermann@med.uni-goettingen.de\t\t \r\n\t\t German Center for Neurodegenerative Diseases (DZNE), 37075 Göttingen, Germany, peter.hermann@med.uni-goettingen.de"],["dc.contributor.affiliation","Zerr, Inga; \t\t \r\n\t\t Department of Neurology, Clinical Dementia Center, University Medical School, Georg-August University, 37075 Göttingen, Germany, IngaZerr@med.uni-goettingen.de\t\t \r\n\t\t German Center for Neurodegenerative Diseases (DZNE), 37075 Göttingen, Germany, IngaZerr@med.uni-goettingen.de"],["dc.contributor.affiliation","Trullas, Ramon; \t\t \r\n\t\t Neurobiology Unit, Institut d’Investigacions Biomèdiques de Barcelona (CSIC), 08036 Barcelona, Spain, ramon.trullas@iibb.csic.es\t\t \r\n\t\t Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), 08036 Barcelona, Spain, ramon.trullas@iibb.csic.es\t\t \r\n\t\t Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), 08036 Barcelona, Spain, ramon.trullas@iibb.csic.es"],["dc.contributor.author","Podlesniy, Petar"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Puigròs, Margalida"],["dc.contributor.author","Serra, Nuria"],["dc.contributor.author","Sepúlveda-Falla, Diego"],["dc.contributor.author","Schmidt, Christian"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Trullas, Ramon"],["dc.date.accessioned","2021-04-14T08:32:33Z"],["dc.date.available","2021-04-14T08:32:33Z"],["dc.date.issued","2020"],["dc.date.updated","2022-09-07T00:35:16Z"],["dc.identifier.doi","10.3390/ijms21176298"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83949"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Cerebrospinal Fluid Mitochondrial DNA in Rapid and Slow Progressive Forms of Alzheimer’s Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","290"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Biomolecules"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Villar-Piqué, Anna"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Calero, Olga"],["dc.contributor.author","Stehmann, Christiane"],["dc.contributor.author","Sarros, Shannon"],["dc.contributor.author","Moda, Fabio"],["dc.contributor.author","Ferrer, Isidre"],["dc.contributor.author","Poleggi, Anna"],["dc.contributor.author","Pocchiari, Maurizio"],["dc.contributor.author","Catania, Marcella"],["dc.contributor.author","Klotz, Sigrid"],["dc.contributor.author","O’Regan, Carl"],["dc.contributor.author","Brett, Francesca"],["dc.contributor.author","Heffernan, Josephine"],["dc.contributor.author","Ladogana, Anna"],["dc.contributor.author","Collins, Steven J."],["dc.contributor.author","Calero, Miguel"],["dc.contributor.author","Kovacs, Gabor G."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2020-12-10T18:46:57Z"],["dc.date.available","2020-12-10T18:46:57Z"],["dc.date.issued","2020"],["dc.description.sponsorship","Instituto de Salud Carlos III"],["dc.identifier.doi","10.3390/biom10020290"],["dc.identifier.eissn","2218-273X"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17338"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78594"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","MDPI"],["dc.relation.eissn","2218-273X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Diagnostic Accuracy of Prion Disease Biomarkers in Iatrogenic Creutzfeldt-Jakob Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["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.firstpage","841"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","859"],["dc.bibliographiccitation.volume","141"],["dc.contributor.author","Diaz-Lucena, Daniela"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Thüne, Katrin"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Villar-Piqué, Anna"],["dc.contributor.author","da Cunha, Jose Eriton Gomes"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","López-Pérez, Óscar"],["dc.contributor.author","Andrés-Benito, Pol"],["dc.contributor.author","Llorens, Franc"],["dc.date.accessioned","2021-06-01T09:42:50Z"],["dc.date.available","2021-06-01T09:42:50Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract Triggering receptor expressed on myeloid cells 2 (TREM2) is an innate immune cell surface receptor that regulates microglial function and is involved in the pathophysiology of several neurodegenerative diseases. Its soluble form (sTREM2) results from shedding of the TREM2 ectodomain. The role of TREM2 in prion diseases, a group of rapidly progressive dementias remains to be elucidated. In the present study, we analysed the expression of TREM2 and its main sheddase ADAM10 in the brain of sporadic Creutzfeldt-Jakob disease (sCJD) patients and evaluated the role of CSF and plasma sTREM2 as a potential diagnostic marker of prion disease. Our data indicate that, compared to controls, TREM2 is increased in sCJD patient brains at the mRNA and protein levels in a regional and subtype dependent fashion, and expressed in a subpopulation of microglia. In contrast, ADAM10 is increased at the protein, but not the mRNA level, with a restricted neuronal expression. Elevated CSF sTREM2 is found in sCJD, genetic CJD with mutations E200K and V210I in the prion protein gene ( PRNP ), and iatrogenic CJD, as compared to healthy controls (HC) (AUC = 0.78–0.90) and neurological controls (AUC = 0.73–0.85), while CSF sTREM2 is unchanged in fatal familial insomnia. sTREM2 in the CSF of cases with Alzheimer’s disease, and multiple sclerosis was not significantly altered in our series. CSF sTREM2 concentrations in sCJD are PRNP codon 129 and subtype-related, correlate with CSF 14-3-3 positivity, total-tau and YKL-40, and increase with disease progression. In plasma, sTREM2 is increased in sCJD compared with HC (AUC = 0.80), displaying positive correlations with plasma total-tau, neurofilament light, and YKL-40. We conclude that comparative study of TREM2 in brain and biological fluids of prion diseases reveals TREM2 to be altered in human prion diseases with a potential value in target engagement, patient stratification, and disease monitoring."],["dc.identifier.doi","10.1007/s00401-021-02296-1"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85371"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.title","TREM2 expression in the brain and biological fluids in prion diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["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.journal","Molecular Neurobiology"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Canaslan, Sezgi"],["dc.contributor.author","Espinosa, Juan Carlos"],["dc.contributor.author","Fernández-Borges, Natalia"],["dc.contributor.author","Villar-Piqué, Anna"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Varges, Daniela"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Torres, Juan Maria"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2022-07-01T07:35:38Z"],["dc.date.available","2022-07-01T07:35:38Z"],["dc.date.issued","2022"],["dc.description.sponsorship"," Fundació La Marató de TV3 http://dx.doi.org/10.13039/100008666"],["dc.description.sponsorship"," Alzheimer Forschung Initiative http://dx.doi.org/10.13039/100010146"],["dc.description.sponsorship","Robert Koch-Institute through funds of the Federal Ministry of Health"],["dc.description.sponsorship","CJD Foundation"],["dc.identifier.doi","10.1007/s12035-022-02891-7"],["dc.identifier.pii","2891"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112222"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-581"],["dc.relation.eissn","1559-1182"],["dc.relation.issn","0893-7648"],["dc.rights.uri","https://www.springer.com/tdm"],["dc.title","Validation of Plasma and CSF Neurofilament Light Chain as an Early Marker for Sporadic Creutzfeldt-Jakob Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Brain"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Villar-Piqué, Anna"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Escaramís, Geòrgia"],["dc.contributor.author","Calero, Miguel"],["dc.contributor.author","Chen, Cao"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Cramm, Maria"],["dc.contributor.author","Golanska, Ewa"],["dc.contributor.author","Sikorska, Beata"],["dc.contributor.author","Llorens, Franc"],["dc.date.accessioned","2022-04-01T10:00:37Z"],["dc.date.available","2022-04-01T10:00:37Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract Genetic prion diseases are a rare and diverse group of fatal neurodegenerative disorders caused by pathogenic sequence variations in the prion protein gene, PRNP. Data on CSF biomarkers in patients with genetic prion diseases are limited and conflicting results have been reported for unclear reasons. Here, we aimed to analyse the diagnostic accuracy of CSF biomarkers currently used in prion clinical diagnosis in 302 symptomatic genetic prion disease cases from 11 prion diagnostic centres, encompassing a total of 36 different pathogenic sequence variations within the open reading frame of PRNP. CSF samples were assessed for the surrogate markers of neurodegeneration, 14-3-3 protein (14-3-3), total-tau protein (t-tau) and α-synuclein and for prion seeding activity through the real-time quaking-induced conversion assay. Biomarker results were compared with those obtained in healthy and neurological controls. For the most prevalent PRNP pathogenic sequence variations, biomarker accuracy and associations between biomarkers, demographic and genetic determinants were assessed. Additionally, the prognostic value of biomarkers for predicting total disease duration from symptom onset to death was investigated. High sensitivity of the four biomarkers was detected for genetic Creutzfeldt–Jakob disease associated with the E200K and V210I mutations, but low sensitivity was observed for mutations associated with Gerstmann–Sträussler–Scheinker syndrome and fatal familial insomnia. All biomarkers showed good to excellent specificity using the standard cut-offs often used for sporadic Creutzfeldt–Jakob disease. In genetic prion diseases related to octapeptide repeat insertions, the biomarker sensitivity correlated with the number of repeats. New genetic prion disease-specific cut-offs for 14-3-3, t-tau and α-synuclein were calculated. Disease duration in genetic Creutzfeldt–Jakob disease-E200K, Gerstmann–Sträussler–Scheinker-P102L and fatal familial insomnia was highly dependent on PRNP codon 129 MV polymorphism and was significantly associated with biomarker levels. In a large cohort of genetic prion diseases, the simultaneous analysis of CSF prion disease biomarkers allowed the determination of new mutation-specific cut-offs improving the discrimination of genetic prion disease cases and unveiled genetic prion disease-specific associations with disease duration."],["dc.identifier.doi","10.1093/brain/awab350"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105472"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","1460-2156"],["dc.relation.issn","0006-8950"],["dc.title","Diagnostic accuracy of cerebrospinal fluid biomarkers in genetic prion diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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","3476"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.bibliographiccitation.lastpage","3483"],["dc.bibliographiccitation.volume","56"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Villar-Piqué, Anna"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Gmitterová, Karin"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Varges, Daniela"],["dc.contributor.author","Zafar, Saima"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Vanderstichele, Hugo"],["dc.contributor.author","Demeyer, Leentje"],["dc.contributor.author","Stoops, Erik"],["dc.contributor.author","Trojanowski, John Q"],["dc.contributor.author","Lee, Virginia M-Y"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2020-12-10T14:14:28Z"],["dc.date.available","2020-12-10T14:14:28Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1007/s12035-018-1313-4"],["dc.identifier.eissn","1559-1182"],["dc.identifier.issn","0893-7648"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71351"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Cerebrospinal Fluid Total and Phosphorylated α-Synuclein in Patients with Creutzfeldt–Jakob Disease and Synucleinopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","289"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Frontiers in aging neuroscience"],["dc.bibliographiccitation.lastpage","9"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Knipper, Tobias"],["dc.contributor.author","Schmidt, Christian"],["dc.contributor.author","Lange, Peter"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-01-09T14:55:23Z"],["dc.date.available","2018-01-09T14:55:23Z"],["dc.date.issued","2017"],["dc.description.abstract","Vascular factors increase the risks of developing Alzheimer's disease (AD) and they contribute to AD pathology. Since amyloid beta (Aβ) deposits can be observed in both diseases, there is an overlap which impedes a clear discrimination and difficult clinical diagnosis. In the present study, we compared cerebrospinal fluid (CSF) profiles of neurodegenerative and inflammatory biomarkers in a patient cohort of controls (n = 50), AD (n = 65) and vascular dementia (VaD) (n = 31) cases. Main results were validated in a second cohort composed of AD (n = 26), rapidly progressive AD (rpAD) (n = 15), VaD (n = 21), and cognitively unimpaired patients with vascular encephalopathy (VE) (n = 25) cases. In the study, cohort significant differences were detected in tau, p-tau, and Aβ1-42 (Aβ42) levels between AD and VaD patients, but not for the neuron-specific enolase (NSE), S100B protein, 14-3-3 and YKL-40. Differential tau, p-tau, and Aβ42 levels between AD and VaD were confirmed in the validation cohort, which additionally showed no differences between AD and rpAD, nor between VaD and VE. The evaluation of the biomarker performance in discrimination between AD and VaD patients revealed that the best diagnostic accuracy could be obtained when tau, p-tau, and Aβ42 were combined in form of Aβ42/p-tau (AUC 0.84-0.90, sensitivity 77-81%, specificity 80-93%) and (tau × p-tau)/Aβ42 ratio (AUC 0.83-0.87, sensitivity 73-81%, specificity 78-87%). Altogether, our studies provided neurodegenerative biomarker profiles in two cohorts of AD and VaD patients favoring the combination of CSF biomarker to differentiate between diseases."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.3389/fnagi.2017.00289"],["dc.identifier.pmid","28955218"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14625"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11611"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Cerebrospinal Fluid Biomarkers of Alzheimer's Disease Show Different but Partially Overlapping Profile Compared to Vascular Dementia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]