Hermann, Peter

[["dc.bibliographiccitation.firstpage","1182"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Intensive Care Medicine"],["dc.bibliographiccitation.lastpage","1191"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Heuer, J. F."],["dc.contributor.author","Pelosi, Paolo"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Crozier, Thomas A."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Quintel, Michael"],["dc.date.accessioned","2018-11-07T08:54:47Z"],["dc.date.available","2018-11-07T08:54:47Z"],["dc.date.issued","2011"],["dc.description.abstract","To determine reciprocal and synergistic effects of acute intracranial hypertension and ARDS on neuronal and pulmonary damage and to define possible mechanisms. Twenty-eight mechanically ventilated pigs were randomized to four groups of seven each: control; acute intracranial hypertension (AICH); acute respiratory distress syndrome (ARDS); acute respiratory distress syndrome in combination with acute intracranial hypertension (ARDS + AICH). AICH was induced with an intracranial balloon catheter and the inflation volume was adjusted to keep intracranial pressure (ICP) at 30-40 cmH(2)O. ARDS was induced by oleic acid infusion. Respiratory function, hemodynamics, extravascular lung water index (ELWI), lung and brain computed tomography (CT) scans, as well as inflammatory mediators, S100B, and neuronal serum enolase (NSE) were measured over a 4-h period. Lung and brain tissue were collected and examined at the end of the experiment. In both healthy and injured lungs, AICH caused increases in NSE and TNF-alpha plasma concentrations, extravascular lung water, and lung density in CT, the extent of poorly aerated (dystelectatic) and atelectatic lung regions, and an increase in the brain tissue water content. ARDS and AICH in combination induced damage in the hippocampus and decreased density in brain CT. AICH induces lung injury and also exacerbates pre-existing damage. Increased extravascular lung water is an early marker. ARDS has a detrimental effect on the brain and acts synergistically with intracranial hypertension to cause histological hippocampal damage."],["dc.identifier.doi","10.1007/s00134-011-2232-2"],["dc.identifier.isi","000292286800020"],["dc.identifier.pmid","21544692"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7288"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22752"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0342-4642"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Acute effects of intracranial hypertension and ARDS on pulmonary and neuronal damage: a randomized experimental study in pigs"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["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","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.artnumber","e105000"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Romero, Carlos"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Reis, Clemens"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:36:27Z"],["dc.date.available","2018-11-07T09:36:27Z"],["dc.date.issued","2014"],["dc.description.abstract","Despite existing criteria, differential diagnosis of Vascular Dementia (VD) and Alzheimer's disease (AD) remains difficult. The aim of this study is to figure out cognitive and biomarker profiles that may help to distinguish between VD, AD and AD + Cerebral Small Vessel Disease (CSVD). We examined a cohort of patients with CSVD (n = 92). After stratification of cognitive impaired patients (n = 59) using the standard CSF beta-amyloid 42/40 ratio cut-off point of 0.975, we obtained two groups which differed with respect to several features: 32 patients with normal beta-amyloid 42/40 ratio (>0.975) showed markedly impaired blood-brain-barrier function as indicated by an elevated albumin ratio (median 8.35). They also differed in cognitive profiles when compared to 27 patients with AD typical beta-amyloid ratio and normal albumin ratio. We also enrolled an additional group of patients with AD (no significant CSVD on MRI, n = 27) which showed no impairment of the blood-brain-barrier. We showed a negative correlation between the albumin ratio and executive cognitive function (p = 0.016) and a negative correlation between memory function and typical AD markers like Tau (p = 0.004) and p181-Tau (p = 0.023) in our cohort. We suppose that the group of patients with normal beta-amyloid ratio represents VD while patients in the other groups represent AD+CSVD and pure AD. Our results support the idea that a dysfunction of the blood-brain-barrier might be contributing factor in the development of cognitive decline in CSVD as it seems to be of more importance than the severity of white matter lesions."],["dc.description.sponsorship","mobility exchange program BMBF [ARG 07/008]"],["dc.identifier.doi","10.1371/journal.pone.0105000"],["dc.identifier.isi","000341230600030"],["dc.identifier.pmid","25147945"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10786"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32623"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","CSF Biomarkers and Neuropsychological Profiles in Patients with Cerebral Small-Vessel Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["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.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"]]

[["dc.bibliographiccitation.journal","Frontiers in Neurology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.affiliation","Maass, Fabian; 1Department of Neurology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Hermann, Peter; 1Department of Neurology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Varges, Daniela; 1Department of Neurology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Nuhn, Sabine; 1Department of Neurology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","van Riesen, Christoph; 1Department of Neurology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Jamous, Ala; 3Department of Neuroradiology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Focke, Niels K.; 1Department of Neurology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Hewitt, Manuel; 1Department of Neurology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Leha, Andreas; 4Department of Medical Statistics, University Medical Center, Göttingen, Germany"],["dc.contributor.affiliation","Bähr, Mathias; 1Department of Neurology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Zerr, Inga; 1Department of Neurology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Varges, Daniela"],["dc.contributor.author","Nuhn, Sabine"],["dc.contributor.author","van Riesen, Christoph"],["dc.contributor.author","Jamous, Ala"],["dc.contributor.author","Focke, Niels K."],["dc.contributor.author","Hewitt, Manuel"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2022-08-04T08:31:14Z"],["dc.date.available","2022-08-04T08:31:14Z"],["dc.date.issued","2022-07-19"],["dc.date.updated","2022-08-02T14:39:19Z"],["dc.description.abstract","The objective of the study was to characterize the pattern of cognitive dysfunction in patients with multiple system atrophy (MSA) applying a standardized neuropsychological assessment. A total of 20 patients with the diagnosis of probable or possible MSA were enrolled for neuropsychological assessment applying the CERAD plus battery. All patients were tested at baseline and 14/20 patients received additional follow-up assessments (median follow-up of 24 months). Additionally, relationship between cortical thickness values/subcortical gray matter volumes and CERAD subitems was evaluated at baseline in a subgroup of 13/20 patients. Trail Making Test (TMT) was the most sensitive CERAD item at baseline with abnormal performance (z-score < −1.28) in one or both pathological TMT items (TMT-A, TMT-B) in 60% of patients with MSA. Additionally, there was a significant inverse correlation between the volume of the left and the right accumbens area and the TMT A item after adjusting for age (left side: p = 0.0009; right side p = 0.003). Comparing both subtypes, patients with MSA-C had significant lower values in phonemic verbal fluency (p = 0.04) and a trend for lower values in semantic verbal fluency (p = 0.06) compared to MSA-P. Additionally, patients with MSA-C showed significantly worse performance in the TMT-B task (p = 0.04) and a trend for worse performance in the TMT-A task (p = 0.06). Concerning longitudinal follow-up, a significant worsening in the TMT-B (p = 0.03) can be reported in MSA. In conclusion, frontal-executive dysfunction presents the hallmark of cognitive impairment in MSA."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3389/fneur.2022.881369"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112628"],["dc.language.iso","en"],["dc.relation.eissn","1664-2295"],["dc.rights","CC BY 4.0"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Prospective CERAD Neuropsychological Assessment in Patients With Multiple System Atrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["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"]]