Schmidt, Christian D.

[["dc.bibliographiccitation.firstpage","189"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Alzheimer s Disease"],["dc.bibliographiccitation.lastpage","196"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Gerlach, Nicole"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Thom, Tobias"],["dc.contributor.author","Kramer, Katharina"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T10:02:58Z"],["dc.date.available","2018-11-07T10:02:58Z"],["dc.date.issued","2015"],["dc.description.abstract","Background/Objective: Apolipoprotein E (ApoE) has an active part in the pathogenesis of Alzheimer's disease (AD). Cerebrospinal fluid (CSF) and plasma level alterations have been reported in AD patients. In search of a biomarker potentially predictive of cognitive, functional, or motor decline, we analyzed the CSF to serum ratios of ApoE levels (CSF/serum ApoE) in AD patients in this regard. Methods: Subjects with newly diagnosed AD were followed within a longitudinal observational study (rpAD study). Annual neuropsychological testing and physical examination were performed. Multiple regression analyses were used to determine possible associations of the ApoE CSF/serum concentration ratios and velocity of decline on a variety of cognitive, functional and motor scales (MMSE, iADL, bADL, GDS, UPDRSIII) adjusted for relevant co-variables. Results: CSF/serum ratios of ApoE levels were associated with progression on the UPDRSIII (change of UPDRSIII slope [pt/yr] per unit of ApoE CSF/serum = -0.06, p < 0.01) and instrumental ADL scale (change of iADL slope [pt/yr] per unit of ApoE CSF/serum = 0.01, p = 0.01) (\"the lower the ratio, the faster the deterioration\" and vice versa). Secondarily, higher age at onset was associated with faster UPDRSIII progression, antidepressant use with faster iADL decline, and better baseline function with more rapid decline on either MMSE, iADL, or GDS scale. Conclusion: Here, CSF/serum ApoE at time of AD diagnosis was shown to be inversely associated with medium-term functional and motor progression. Whether this ratio qualifies for the use as a predictive biomarker must be validated in larger cohort studies over the long term."],["dc.description.sponsorship","Bundesministerium fur Bildung und Forschung (BMBF) [01GI1010C, KNDD-2]"],["dc.identifier.doi","10.3233/JAD-150286"],["dc.identifier.isi","000360931700017"],["dc.identifier.pmid","26401939"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38342"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ios Press"],["dc.relation.issn","1875-8908"],["dc.relation.issn","1387-2877"],["dc.title","Baseline CSF/Serum-Ratio of Apolipoprotein E and Rate of Differential Decline in Alzheimer's Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Stoeck, Katharina"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:26:11Z"],["dc.date.available","2018-11-07T09:26:11Z"],["dc.date.issued","2013"],["dc.format.extent","58"],["dc.identifier.isi","000323217500134"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30244"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.publisher.place","Austin"],["dc.relation.issn","1933-6896"],["dc.title","Immune responses in rapid dementia: A comparative study on neuroinflammatory markers in CJD, AD, rpAD and MS patients"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","577"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Alzheimer s & Dementia"],["dc.bibliographiccitation.lastpage","589"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Karch, Andre"],["dc.contributor.author","Cramm, Maria"],["dc.contributor.author","Lange, Peter"],["dc.contributor.author","Gherib, Kerim"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Stoeck, Katharina"],["dc.date.accessioned","2018-11-07T10:14:52Z"],["dc.date.available","2018-11-07T10:14:52Z"],["dc.date.issued","2016"],["dc.description.abstract","Introduction: The analysis of cerebrospinal fluid biomarkers gains importance in clinical routine and is effective in substantiating dementia diagnosis in the differential diagnostic context. Methods: We evaluated the levels of beta-amyloid (A beta) 42, A beta 40, tau, and P-tau in a large patient population subdivided into prion diseases, tauopathies, synucleinopathies, and controls. Diagnostic test evaluation was assessed by ROC area under the curve analysis. Results: High tau levels were detected in sporadic Creutzfeldt-Jakob disease (sCJD) and high P-tau levels in Alzheimer's disease (AD) and sCJD. A beta 40 was lower exclusively in prionopathies, but low A beta 42 was detected in AD, sCJD, and Lewy body dementia. When disease groups were stratified according to the underlying proteinopathy, we detected disease-type specificities for all biomarkers. P-tau/tau, A beta 42/40, A beta 42/tau, and A beta 40/tau ratios proved valuable in discriminating disease groups and controls, especially P-tau/tau ratio in the identification of sCJD cases. Discussion: Combining the biomarker panel allows differentiating between various types of neuro-degenerative dementias and contributes to a better understanding of their pathophysiological processes. (C) 2015 Alzheimer's Association. Published by Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.jalz.2015.10.009"],["dc.identifier.isi","000376054200007"],["dc.identifier.pmid","26718584"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40704"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","1552-5279"],["dc.relation.issn","1552-5260"],["dc.title","Comparative analysis of cerebrospinal fluid biomarkers in the differential diagnosis of neurodegenerative dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","151"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","152"],["dc.bibliographiccitation.volume","253"],["dc.contributor.author","Stoeck, Katharina"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:02:17Z"],["dc.date.available","2018-11-07T09:02:17Z"],["dc.date.issued","2012"],["dc.identifier.isi","000312764800407"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24645"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","11th International Congress of Neuroimmunology (ISNI)"],["dc.relation.eventlocation","Boston, MA"],["dc.relation.issn","0165-5728"],["dc.title","Immune responses in rapid dementia - A comparative study on neuroinflammatory markers in CJD, AD, rpAD and MS patients"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","170"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Stoeck, Katharina"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Ebert, Elisabeth"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:33:33Z"],["dc.date.available","2018-11-07T09:33:33Z"],["dc.date.issued","2014"],["dc.description.abstract","Immunological responses may contribute to disease progression and clinical heterogeneity in neurodegenerative dementia, for example, Alzheimer's disease (AD) and Creutzfeldt-Jakob disease (CJD). Recently, a rapidly progressive form of AD (rpAD) has been described. On neuropathological grounds classical AD and rpAD are not distinguishable at present. All those protein aggregopathies show a state of chronic inflammation with microglia activation and production of proinflammatory cytokines. In this context, it is hypothesized that the severity of the surrounding inflammation substantially contributes to disease progression and accelerated disease courses as seen in rpAD. Using a cytokine multiplex array based on Luminex Technology, we studied 17 pro-and anti-inflammatory cytokines in cerebrospinal fluid (CSF) and serum from patients with classical dementia (AD) or rapidly progressive dementia (Creutzfeldt-Jakob disease (CJD), rpAD). For controls, we chose patients with multiple sclerosis (MS) and non-neurodegenerative diseases. We found a significant and isolated elevation of proinflammatory cytokines (IL-13, TNF-alpha and G-CSF) in the serum of rpAD patients. In CSF, IL-8 and MCP-1 chemokines were significantly elevated in CJD patients and MCP-1 in AD patients. In conclusion, we found a characteristic proinflammatory cytokine response in the serum of rpAD patients. It might explain the more rapidly progressive course of the rpAD subform and can be helpful in distinguishing between classical AD and rpAD."],["dc.identifier.doi","10.1186/s12974-014-0170-y"],["dc.identifier.isi","000346026300001"],["dc.identifier.pmid","25315814"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11001"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31989"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1742-2094"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Immune responses in rapidly progressive dementia: a comparative study of neuroinflammatory markers in Creutzfeldt-Jakob disease, Alzheimer's disease and multiple sclerosis"],["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","2597"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Neurobiology of Aging"],["dc.bibliographiccitation.lastpage","2606"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Oikonomou, Pantelis"],["dc.contributor.author","Stoeck, Katharina"],["dc.contributor.author","Ebert, Elisabeth"],["dc.contributor.author","Poliakova, Tatjana"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Zafar, Saima"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:53:04Z"],["dc.date.available","2018-11-07T09:53:04Z"],["dc.date.issued","2015"],["dc.description.abstract","Understanding inflammatory mechanisms in vascular dementia (VD) is pivotal for achieving better insights into changes in brain metabolism. We performed cytokine profiling and measured levels of the cellular prion protein (PrPC) in serum and cerebrospinal fluid (CSF) samples from patients with VD and with vascular encephalopathy (VE). Significant changes were observed for interleukin (IL)-1 beta, IL-4, IL-5, tumor necrosis factor alpha, interferon gamma, granulocyte-colony stimulating factor, monocyte chemotactic protein 1, and macrophage inflammatory protein 1 beta in serum and for IL-6 and granulocyte macrophage colony-stimulating factor in CSF of VD and VE patients, suggesting that most of immune markers depend on vascular lesions, while only IL-6 was related to dementia. In VD patients, the severity of dementia as defined by the Mini-Mental Status Test or Cambridge Cognitive Examination battery test was significantly correlated with the levels of IL-8 (CSF) and macrophage inflammatory protein 1 beta (serum and CSF). Additionally, in CSF of VD patients, our data revealed a correlation between immune and neurodegenerative marker proteins. Both indicate an association of neuroinflammation and cognitive decline. Levels of PrPC were regulated differentially in VD and VE patients compared with Alzheimer's disease patients and controls. Moreover, we observed a significant negative correlation between cytokine levels and PrPC in VD patients in CSF and serum, as well as a correlation between PrPC expression with levels of neurodegenerative marker proteins in CSF (in VD and VE patients). Our data suggest that immunological modifiers play a role in VD and VE patients and provide evidence for an association of PrPC with immune and neurodegenerative markers. (C) 2015 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.neurobiolaging.2015.05.013"],["dc.identifier.isi","000358803400016"],["dc.identifier.pmid","26170132"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36250"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","1558-1497"],["dc.relation.issn","0197-4580"],["dc.title","Cytokine profiles and the role of cellular prion protein in patients with vascular dementia and vascular encephalopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","398"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of the Neurological Sciences"],["dc.bibliographiccitation.lastpage","403"],["dc.bibliographiccitation.volume","358"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Gloeckner, Sara Friederike"],["dc.contributor.author","Kaerst, Lisa"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:48:55Z"],["dc.date.available","2018-11-07T09:48:55Z"],["dc.date.issued","2015"],["dc.description.abstract","Background: Alterations in the CSF/serum albumin ratio (Qalb) is currently recognized as one of the most reliable markers of blood-brain barrier impairment and blood-CSF barrier permeability, but its potential role as a biomarker in the differential diagnosis of neurological diseases has been poorly analysed. Methods: We evaluated Qalb and core CSF biomarkers (Tau, p-Tau and A beta 42) in a large patient population of neurological and neurodegenerative cases. Diagnostic test evaluation was assessed by ROC-AUC analysis. Results: In the differential diagnostic analysis, increased Qalb was found in dementia with Lewy bodies (DLB) patients compared to other diseases, either individually or stratified in non-dementia and dementia groups. When clinical groups were analysed individually and compared to controls, Qalb was also increased in stroke and Parkinson's disease dementia (PDD) cases, but not in Parkinson's disease (PD). Qalb in DLB cases correlate with CSF A beta 42 levels but not with Tau and p-Tau levels. Due to the lower CSF A beta 42 levels in DLB compared to PD and PDD, the potential clinical applicability of Qalb with respect to the DLB diagnosis is increased in combination with CSF A beta 42 analysis. Conclusions: The present study demonstrates increased Qalb in synucleinopathies associated with dementia revealing a potential new clinical approach for the differential diagnosis of DLB. (C) 2015 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jns.2015.10.011"],["dc.identifier.isi","000365050200065"],["dc.identifier.pmid","26476775"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35404"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1878-5883"],["dc.relation.issn","0022-510X"],["dc.title","Increased albumin CSF/serum ratio in dementia with Lewy bodies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]