Schmidt, Christian D.

[["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.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.artnumber","e84405"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Karch, Andre"],["dc.contributor.author","Manthey, Henrike"],["dc.contributor.author","Ponto, Claudia"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Heinemann, Uta"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:16:26Z"],["dc.date.available","2018-11-07T09:16:26Z"],["dc.date.issued","2013"],["dc.description.abstract","Background: Since more than a decade ApoE is known to be a strong risk factor for Alzheimer's disease (AD); however, molecular pathways mediating this risk are still unclear. In recent years it has been hypothesized that ApoE might play a role in the disintegration of blood-brain barrier (BBB). In the present study we addressed the question if ApoE genotypes might be associated with BBB function measured by albumin ratio (Q(Alb)) in a large cohort of patients with different types of dementia. Methods: Five hundred twenty (520) patients with Creutzfeldt-Jakob disease (CJD, n = 350), Alzheimer's disease (n = 71) and cerebral small vessel disease (n = 99) were assessed for their ApoE genotype. BBB function was measured in all patients using Q(Alb) and was compared between ApoE genotypes. Dominant and additive genetic models were assumed in order to investigate the potential effect of ApoE on BBB function. Results: We observed no systematic differences in Q(Alb) between ApoE genotypes within the present study. Increased Q(Alb) levels were shown for those without E3 allele in the subgroup of CJD patients when assuming a dominant genetic model (p = 0.035). This could not be confirmed for patients with other forms of dementia (p = 0.234). Discussion: Although there was some evidence for a protective effect of E3 alleles in CJD patients, this study does not support the hypothesis of a systematic role of ApoE genotypes in BBB function in individuals with a diagnosis of dementia. Thus, changes in BBB function do not seem to contribute to the increased risk of cognitive decline associated with certain ApoE genotypes. The interpretation of the results of this study must take into account that BBB function was only assessed by measuring Q(Alb) which has been shown to be a good marker for overall BBB integrity but might not reflect all qualities of the barrier."],["dc.identifier.doi","10.1371/journal.pone.0084405"],["dc.identifier.isi","000329117900091"],["dc.identifier.pmid","24386372"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9577"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27934"],["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 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Investigating the Association of ApoE Genotypes with Blood-Brain Barrier Dysfunction Measured by Cerebrospinal Fluid-Serum Albumin Ratio in a Cohort of Patients with Different Types of Dementia"],["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"]]