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Hermann, Peter
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Hermann, Peter
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Hermann, Peter
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Hermann, P.
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2011Journal Article [["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"]]Details DOI PMID PMC WOS2020Journal Article Research Paper [["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"]]Details DOI2018Journal Article [["dc.bibliographiccitation.firstpage","761"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Expert Review of Neurotherapeutics"],["dc.bibliographiccitation.lastpage","772"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Hermann, Peter"],["dc.date.accessioned","2020-12-10T18:15:09Z"],["dc.date.available","2020-12-10T18:15:09Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1080/14737175.2018.1519397"],["dc.identifier.eissn","1744-8360"],["dc.identifier.issn","1473-7175"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/74764"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Diagnostic challenges in rapidly progressive dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2016Journal Article [["dc.bibliographiccitation.firstpage","743"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","MINERVA ANESTESIOLOGICA"],["dc.bibliographiccitation.lastpage","750"],["dc.bibliographiccitation.volume","82"],["dc.contributor.author","Harnisch, Lars-Olav"],["dc.contributor.author","Zippel, Carsten"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Quintel, Michael"],["dc.contributor.author","Moerer, Onnen"],["dc.date.accessioned","2018-11-07T10:11:48Z"],["dc.date.available","2018-11-07T10:11:48Z"],["dc.date.issued","2016"],["dc.description.abstract","BACKGROUND: Patient-ventilator asynchrony that prolongs weaning and increases morbidity and mortality is common during invasive ventilation of patients with chronic obstructive pulmonary disease (COPD). In this context, the inspiratory cycling criteria (iCC) of the ventilator during assisted pressure support (PS) ventilation is a poorly acknowledged key factor. We investigated the changes of flow and pressure parameters that resulted from varying the iCC in a simulated COPD lung model. METHODS: A lung simulator was connected to an ICU ventilator through an endotracheal tube. We studied iCC settings from 10% to 70% at different respiratory rates (RR) (15 and 30 bpm) and pressure support (PS) (5 and 15 cmH(2)O) settings and registered asynchrony-index, double-triggering, expiratory trigger latency (TLEXP), intrinsic PEEP (PEEPi), expiratory pressure time product (PTPEXP) and tidal volume. RESULTS: At iCC <= 20%, asynchrony occurred in 50% of all recordings in high RR/high PS. At a low RR, double triggering occurred at high iCC settings. It appeared at 50% iCC with low PS and at 60% iCC with high PS. TLEXP was positive at iCC 10% to 30% but decreased with increasing iCC (P< 0.001). At low RR/high PS settings, PEEPi decreased at iCC <= 40% but increased at iCC >= 50%. High RR/low PS constantly reduced PTPEXP up to 60% iCC. Changes in iCC strongly influenced the resulting tidal volume. CONCLUSIONS: Non-adapted ventilator iCC can cause patient-ventilator asynchrony. The success of assisted invasive ventilation and weaning relies on meticulous adjustments."],["dc.description.sponsorship","Faron Pharm."],["dc.identifier.isi","000386888700006"],["dc.identifier.pmid","26630027"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40114"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Edizioni Minerva Medica"],["dc.relation.issn","1827-1596"],["dc.relation.issn","0375-9393"],["dc.title","Adjusting ventilator off-cycling in invasively ventilated COPD patients needs comprehensive adjustments"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details PMID PMC WOS2021Journal Article [["dc.bibliographiccitation.journal","Nature Reviews Neurology"],["dc.contributor.author","Watson, Neil"],["dc.contributor.author","Brandel, Jean-Philippe"],["dc.contributor.author","Green, Alison"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Ladogana, Anna"],["dc.contributor.author","Lindsay, Terri"],["dc.contributor.author","Mackenzie, Janet"],["dc.contributor.author","Pocchiari, Maurizio"],["dc.contributor.author","Smith, Colin"],["dc.contributor.author","Pal, Suvankar"],["dc.date.accessioned","2021-06-01T09:41:41Z"],["dc.date.available","2021-06-01T09:41:41Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1038/s41582-021-00488-7"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85003"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1759-4766"],["dc.relation.issn","1759-4758"],["dc.title","The importance of ongoing international surveillance for Creutzfeldt–Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2020Journal Article [["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"]]Details DOI2022Journal Article [["dc.bibliographiccitation.journal","Nature Reviews Neurology"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2022-06-01T09:39:09Z"],["dc.date.available","2022-06-01T09:39:09Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1038/s41582-022-00659-0"],["dc.identifier.pii","659"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108401"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.eissn","1759-4766"],["dc.relation.issn","1759-4758"],["dc.rights.uri","https://www.springer.com/tdm"],["dc.title","Rapidly progressive dementias — aetiologies, diagnosis and management"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2021-04-21Journal Article [["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"]]Details DOI2021Journal Article [["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"]]Details DOI2022Journal Article Research Paper [["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"]]Details DOI