Schmidt, Christian D.

[["dc.bibliographiccitation.firstpage","371"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","378"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Redyk, Katharina"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Krack, Lennart A."],["dc.contributor.author","von Ahsen, Nico"],["dc.contributor.author","Roeber, Sigrun"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T08:47:31Z"],["dc.date.available","2018-11-07T08:47:31Z"],["dc.date.issued","2010"],["dc.description.abstract","Objective: To characterize clinical features, CSF biomarkers and genetic polymorphisms of patients suffering from a rapidly progressing subtype of Alzheimer's dementia (rpAD). Methods: Retrospective analyses of 32 neuropathologically confirmed cases differentially diagnosed as AD out of a group with rapidly progressive dementia. CSF biomarkers (14-3-3, tau, beta-amyloid 1-42) and genetic markers (PRNP codon 129, apolipoprotein E, ApoE, polymorphism) were determined. Results: Median survival was 26 months, age at onset 73 years. Biomarkers: mean beta-amyloid 1-42: 266 pg/ml, median tau: 491 pg/ml, 14-3-3 positive: 31%. Genetic polymorphisms showed a predominance of methionine homozygosity at PRNP codon 129 and a low frequency of ApoE4 (38%, no homozygous patients). Thirty-five symptoms were studied. Frequent symptoms were myoclonus (75%), disturbed gait (66%) and rigidity (50%). Discussion: rpAD is associated with a diversity of neurological signs even able to mimic Creutz feldt-Jakob disease. Biomarkers and genetic profile differ from those seen in classical AD. The findings on biomarkers, symptomatology and genetics may aid the differential diagnostic process. Copyright (C) 2010 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000278692"],["dc.identifier.isi","000278130700012"],["dc.identifier.pmid","20453509"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9103"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20975"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1420-8008"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Clinical Features of Rapidly Progressive Alzheimer's 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.firstpage","4403"],["dc.bibliographiccitation.issue","39"],["dc.bibliographiccitation.journal","Chemical Communications"],["dc.bibliographiccitation.lastpage","4405"],["dc.bibliographiccitation.volume","49"],["dc.contributor.author","Kaschel, Johannes"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Mumby, Mark"],["dc.contributor.author","Kratzert, Daniel"],["dc.contributor.author","Stalke, Dietmar"],["dc.contributor.author","Werz, Daniel B."],["dc.date.accessioned","2018-11-07T09:30:02Z"],["dc.date.available","2018-11-07T09:30:02Z"],["dc.date.issued","2013"],["dc.description.abstract","Furan-derived donor-acceptor-substituted cyclopropanes were reacted with Lawesson's reagent. Depending on the reaction conditions either bisthiophenes or unprecedented cage-like molecules were obtained. Woollins' reagent always led to the respective selenium-containing cage-like compounds."],["dc.identifier.doi","10.1039/c2cc37631h"],["dc.identifier.isi","000317931500091"],["dc.identifier.pmid","23247108"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10787"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31206"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Royal Soc Chemistry"],["dc.relation.issn","1359-7345"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Donor-acceptor cyclopropanes with Lawesson's and Woollins' reagents: formation of bisthiophenes and unprecedented cage-like molecules"],["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","5"],["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Karch, Andre"],["dc.contributor.author","Korth, Carsten"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:03:55Z"],["dc.date.available","2018-11-07T09:03:55Z"],["dc.date.issued","2012"],["dc.description.abstract","Results from recent experiments with rodents imply that Alzheimer disease might be inducible by seeding A beta peptides into recipient animals. In respect to this new experimental data, public health aspects as well as epidemiological data have to be reevaluated. In this article, the available experimental and epidemiological data are reviewed."],["dc.identifier.doi","10.4161/pri.22502"],["dc.identifier.isi","000311341100008"],["dc.identifier.pmid","23052009"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10653"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24999"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1933-6896"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","On the issue of transmissibility of Alzheimer disease A critical review"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","84"],["dc.bibliographiccitation.issue","2-3"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","89"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Wolff, Martin"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:15:14Z"],["dc.date.available","2018-11-07T09:15:14Z"],["dc.date.issued","2012"],["dc.description.abstract","Background/Aim: To investigate the influence of established genetic risk factors for Alzheimer's disease on the speed of disease progression. Methods: Polymorphisms (in ACE, ApoE, BIN1, CLU, CR1, CST3, EXOC3L2, GWA14q32.13, IL8, LDLR, PICALM, TNK1) of 40 Alzheimer's disease patients from a longitudinal study were analyzed. A standardized loss of Mini-Mental State Examination points was used as the progression parameter. Results: Polymorphisms in CST3 and EXOC3L2 as well as the absence of APOE4 were associated with more aggressive disease courses. A trend was observed for BIN1. Conclusion: In addition to being a risk factor for disease development, some of the polymorphisms investigated here are associated with higher rates of decline and disease progression and thus might act as prognostic disease markers. This effect needs to be considered in future treatment strategies. Copyright (C) 2012 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000336790"],["dc.identifier.isi","000305654800002"],["dc.identifier.pmid","22414550"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9085"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27631"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","S. Karger AG"],["dc.relation.eissn","1421-9824"],["dc.relation.issn","1420-8008"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Alzheimer's Disease: Genetic Polymorphisms and Rate of Decline"],["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","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","e66664"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Goldeck, David"],["dc.contributor.author","Larbi, Anis"],["dc.contributor.author","Pellicano, Mariavaleria"],["dc.contributor.author","Alam, Iftikhar"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Fulop, Tamas"],["dc.contributor.author","Pawelec, Graham"],["dc.date.accessioned","2018-11-07T09:23:38Z"],["dc.date.available","2018-11-07T09:23:38Z"],["dc.date.issued","2013"],["dc.description.abstract","Although primarily a neurological complaint, systemic inflammation is present in Alzheimer's Disease, with higher than normal levels of proinflammatory cytokines and chemokines in the periphery as well as the brain. A gradient of these factors may enhance recruitment of activated immune cells into the brain via chemotaxis. Here, we investigated the phenotypes of circulating immune cells in AD patients with multi-colour flow cytometry to determine whether their expression of chemokine receptors is consistent with this hypothesis. In this study, we confirmed our previously reported data on the shift of early-to late-differentiated CD4+ T-cells in AD patients. The percentage of cells expressing CD25, a marker of acute T-cell activation, was higher in patients than in age-matched controls, and percentages of CCR6+ cells were elevated. This chemokine receptor is primarily expressed on pro-inflammatory memory cells and Th17 cells. The proportion of cells expressing CCR4 (expressed on Th2 cells) and CCR5 (Th1 cells and dendritic cells) was also greater in patients, and was more pronounced on CD4+ than CD8+ T-cells. These findings allow a more detailed insight into the systemic immune status of patients with Alzheimer's disease and suggest possible novel targets for immune therapy."],["dc.identifier.doi","10.1371/journal.pone.0066664"],["dc.identifier.isi","000320576400144"],["dc.identifier.pmid","23824053"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9151"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29626"],["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-NC 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/3.0"],["dc.title","Enhanced Chemokine Receptor Expression on Leukocytes of Patients with Alzheimer's 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","36"],["dc.bibliographiccitation.journal","Proteome Science"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Brase, Jan C."],["dc.contributor.author","Mannsperger, Heiko A."],["dc.contributor.author","Froehlich, Holger"],["dc.contributor.author","Gade, Stephan"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Wiemann, Stefan"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Schlomm, Thorsten"],["dc.contributor.author","Sueltmann, Holger"],["dc.contributor.author","Korf, Ulrike"],["dc.date.accessioned","2018-11-07T08:42:11Z"],["dc.date.available","2018-11-07T08:42:11Z"],["dc.date.issued","2010"],["dc.description.abstract","Background: Reverse phase protein arrays (RPPA) emerged as a useful experimental platform to analyze biological samples in a high-throughput format. Different signal detection methods have been described to generate a quantitative readout on RPPA including the use of fluorescently labeled antibodies. Increasing the sensitivity of RPPA approaches is important since many signaling proteins or posttranslational modifications are present at a low level. Results: A new antibody-mediated signal amplification ( AMSA) strategy relying on sequential incubation steps with fluorescently-labeled secondary antibodies reactive against each other is introduced here. The signal quantification is performed in the near-infrared range. The RPPA-based analysis of 14 endogenous proteins in seven different cell lines demonstrated a strong correlation (r = 0.89) between AMSA and standard NIR detection. Probing serial dilutions of human cancer cell lines with different primary antibodies demonstrated that the new amplification approach improved the limit of detection especially for low abundant target proteins. Conclusions: Antibody-mediated signal amplification is a convenient and cost-effective approach for the robust and specific quantification of low abundant proteins on RPPAs. Contrasting other amplification approaches it allows target protein detection over a large linear range."],["dc.identifier.doi","10.1186/1477-5956-8-36"],["dc.identifier.isi","000280283000001"],["dc.identifier.pmid","20569466"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6025"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19642"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1477-5956"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Increasing the sensitivity of reverse phase protein arrays by antibody-mediated signal amplification"],["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","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.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"]]