Wiltfang, Jens

[["dc.bibliographiccitation.firstpage","366"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Experimental Neurology"],["dc.bibliographiccitation.lastpage","370"],["dc.bibliographiccitation.volume","223"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Vanmechelen, Eugeen"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Buerger, Katharina"],["dc.contributor.author","Hampel, Harald"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Henn, Fritz A."],["dc.contributor.author","Falkai, Peter Gaston"],["dc.contributor.author","Ruether, Eckhart"],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Luckhaus, C. H."],["dc.contributor.author","Perneczky, Robert"],["dc.contributor.author","Schmidtke, K."],["dc.contributor.author","Schroeder, J."],["dc.contributor.author","Kessler, H."],["dc.contributor.author","Pantel, Johannes"],["dc.contributor.author","Gertz, H.-J."],["dc.contributor.author","Vanderstichele, Hugo"],["dc.contributor.author","de Meyer, G."],["dc.contributor.author","Shapiro, F."],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Wiltfang, J."],["dc.date.accessioned","2018-11-07T08:42:36Z"],["dc.date.available","2018-11-07T08:42:36Z"],["dc.date.issued","2010"],["dc.description.abstract","We measured concentrations of to peptides 1-42 and 1-40, and their ratio in plasma of patients carefully categorized clinically and neurochemically as having AD or other dementias with a newly commercially available multiplexing assay, characterized by reasonable laboratory performance (intra-assay imprecision in the range of 1.3-3.8% for A beta 1-42, and 1.8-4.1% for A beta 1-40, inter-assay imprecision for A beta 1-42, A beta 1-40, and A beta 1-42/A beta 1-40 concentration ratio in the range of 2.3-11.5%, 2.2-10.4% and 42-9.7%, respectively). Patients with AD or mild cognitive impairment of AD type (MCI-AD) whose clinical diagnosis was supported with CSF biomarkers (n = 193) had significantly lower A beta 1-42 plasma concentrations (p<0.007), and A beta 1-42/1-40 ratios (p<0.003) compared to patients with other dementias and MCI of other types (n = 64). No significant differences between persons with MCI of AD type and patients with early AD were observed, or between MCI of other types versus patients with early dementia of other types. Our findings reconfirm the hypothesis that alterations of biomarker concentrations occur early in a preclinical AD stage and that these alterations are also reflected in plasma. (C) 2009 Published by Elsevier Inc."],["dc.identifier.doi","10.1016/j.expneurol.2009.07.024"],["dc.identifier.isi","000277743700015"],["dc.identifier.pmid","19664622"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19739"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","0014-4886"],["dc.title","Amyloid beta peptides in plasma in early diagnosis of Alzheimer's disease: A multicenter study with multiplexing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","379"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","386"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Wagner, M."],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Reischies, Friedel M."],["dc.contributor.author","Daerr, M."],["dc.contributor.author","Wolfsgruber, S."],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Popp, J."],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Huell, Michael"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Hampel, Harald"],["dc.contributor.author","Perneczky, Robert"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Luckhaus, C."],["dc.contributor.author","Gertz, H.-J."],["dc.contributor.author","Schroeder, J."],["dc.contributor.author","Pantel, Johannes"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, J."],["dc.date.accessioned","2018-11-07T09:13:50Z"],["dc.date.available","2018-11-07T09:13:50Z"],["dc.date.issued","2012"],["dc.description.abstract","Objective: To compare cued recall measures with other memory and nonmemory tests regarding their association with a biomarker profile indicative of Alzheimer disease (AD) in CSF among patients with mild cognitive impairment (MCI). Methods: Data were obtained by the German Dementia Competence Network. A total of 185 memory clinic patients fulfilling broad criteria for MCI (1 SD deficit in memory tests or in nonmemory tests) were assessed with an extended neuropsychological battery, which included the Free and Cued Selective Reminding Test (FCSRT), the word list learning task from the Consortium to Establish a Registry for Alzheimer's Disease neuropsychological battery (CERAD-NP), and the Logical Memory (LM) paragraph recall test from the Wechsler Memory Scale-Revised. CSF was obtained from all patients. Results: A total of 74 out of 185 subjects with MCI (40%) had a CSF profile consistent with AD (A beta(1-42)/tau ratio; CSF AD + group). FCSRT measures reflecting both free and cued recall discriminated best between CSF AD + and CSF AD - patients, and significantly improved CSF AD classification accuracy, as compared with CERAD delayed recall and LM delayed recall. Conclusions: Cued recall deficits are most closely associated with CSF biomarkers indicative of AD in subjects with MCI. This novel finding complements results from prospective clinical studies and provides further empirical support for cued recall as a specific indicator of prodromal AD, in line with recently proposed research criteria. Neurology (R) 2012; 78: 379-386"],["dc.identifier.doi","10.1212/WNL.0b013e318245f447"],["dc.identifier.isi","000300392000007"],["dc.identifier.pmid","22238414"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27260"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Biomarker validation of a cued recall memory deficit in prodromal Alzheimer disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","872"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Alzheimer's & Dementia"],["dc.bibliographiccitation.lastpage","881"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Louwersheimer, Eva"],["dc.contributor.author","Wolfsgruber, Steffen"],["dc.contributor.author","Espinosa, Ana"],["dc.contributor.author","Lacour, André"],["dc.contributor.author","Heilmann-Heimbach, Stefanie"],["dc.contributor.author","Alegret, Montserrat"],["dc.contributor.author","Hernández, Isabel"],["dc.contributor.author","Rosende-Roca, Maitée"],["dc.contributor.author","Tárraga, Lluís"],["dc.contributor.author","Boada, Mercè"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Frölich, Lutz"],["dc.contributor.author","Hüll, Michael"],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Scherer, Martin"],["dc.contributor.author","Riedel-Heller, Steffi"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Nöthen, Markus M."],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Koene, Ted"],["dc.contributor.author","Scheltens, Philip"],["dc.contributor.author","Holstege, Henne"],["dc.contributor.author","Wagner, Michael"],["dc.contributor.author","Ruiz, Agustín"],["dc.contributor.author","van der Flier, Wiesje M."],["dc.contributor.author","Becker, Tim"],["dc.contributor.author","Ramirez, Alfredo"],["dc.date.accessioned","2017-09-07T11:44:36Z"],["dc.date.available","2017-09-07T11:44:36Z"],["dc.date.issued","2016"],["dc.description.abstract","IntroductionWe evaluated the effect of Alzheimer's disease (AD) susceptibility loci on endophenotypes closely related with AD pathology in patients with mild cognitive impairment (MCI).MethodsWe selected 1730 MCI patients from four independent data sets. Weighted polygenic risk scores (PGS) were constructed of 18 non-apolipoprotein E (APOE) AD risk variants. In addition, we determined APOE genotype. AD endophenotypes were cognitive decline over time and cerebrospinal fluid (CSF) biomarkers (aβ, tau, ptau).ResultsPGS was modestly associated with cognitive decline over time, as measured by mini-mental state examination (MMSE) (β ± SE:−0.24 ± 0.10; P = .012), and with CSF levels of tau and ptau (tau: 1.38 ± 0.36, P = 1.21 × 10−4; ptau: 1.40 ± 0.36, P = 1.02 × 10−4).DiscussionIn MCI, we observed a joint effect of AD susceptibility loci on nonamyloid endophenotypes, suggesting a link of these genetic loci with neuronal degeneration in general rather than with Alzheimer-related amyloid deposition."],["dc.identifier.doi","10.1016/j.jalz.2016.01.006"],["dc.identifier.gro","3151698"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8517"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","1552-5260"],["dc.title","Alzheimer's disease risk variants modulate endophenotypes in mild cognitive impairment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1005"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Alzheimer's Disease"],["dc.bibliographiccitation.lastpage","1015"],["dc.bibliographiccitation.volume","76"],["dc.contributor.author","Fuentes, Manuel"],["dc.contributor.author","Klostermann, Arne"],["dc.contributor.author","Kleineidam, Luca"],["dc.contributor.author","Bauer, Chris"],["dc.contributor.author","Schuchhardt, Johannes"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Frölich, Lutz"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Klöppel, Stefan"],["dc.contributor.author","Schieting, Vera"],["dc.contributor.author","Teipel, Stefan J."],["dc.contributor.author","Wagner, Michael"],["dc.contributor.author","Peters, Oliver"],["dc.date.accessioned","2021-04-14T08:27:21Z"],["dc.date.available","2021-04-14T08:27:21Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.3233/JAD-200230"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82256"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1875-8908"],["dc.relation.issn","1387-2877"],["dc.title","Identification of a Cascade of Changes in Activities of Daily Living Preceding Short-Term Clinical Deterioration in Mild Alzheimer’s Disease Dementia via Lead-Lag Analysis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","68"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","71"],["dc.bibliographiccitation.volume","440"],["dc.contributor.author","Koelsch, Heike"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Dichgans, Martin"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Schulz, Joerg B."],["dc.contributor.author","Schwab, Sibylle G."],["dc.contributor.author","Maier, Wolfgang"],["dc.date.accessioned","2018-11-07T11:12:54Z"],["dc.date.available","2018-11-07T11:12:54Z"],["dc.date.issued","2008"],["dc.description.abstract","SORL1 gene variants were described as risk factors of Alzheimer's disease (AD). We investigated the association of four SORL1 variants with CSF levels of A beta(42) and A beta(40) in 153 AD patients recruited from a multicenter study of the German Competence Net Dementias. Only one SORL1 SNP was associated with altered A beta(42) levels in the single marker analysis (SNP21: p = 0.011), the other SNPs did not show an association with A beta(42) orA beta(40) CSF levels. Haplotype analysis identified a three marker SORL1 haplotype consisting of SNP19 T-allele, SNP21 G-allele and SNP23 A-allele (T/G/A) which was associated with reduced A beta(42) CSF levels in AD patients (p = 0.003). A beta(40) levels were also lower in carriers of this haplotype; however, this did not reach statistical significance (p = 0.15). We found a SORL1 haplotype which was associated with CSF levels of amyloid-P cleavage products, measured as altered levels of A beta(42). Thus our data suggest that: SORL1 gene variants might influence AD pathology. (C) 2008 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neulet.2008.05.049"],["dc.identifier.isi","000257640200016"],["dc.identifier.pmid","18541377"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53768"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","Influence of SORL1 gene variants: Association with CSF amyloid-beta products in probable 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.firstpage","547"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Alzheimer s Disease"],["dc.bibliographiccitation.lastpage","560"],["dc.bibliographiccitation.volume","49"],["dc.contributor.author","Koppara, Alexander"],["dc.contributor.author","Wolfsgruber, Steffen"],["dc.contributor.author","Kleineidam, Luca"],["dc.contributor.author","Schmidtke, Klaus"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Kurz, Alexander"],["dc.contributor.author","Schulz, Stefanie"],["dc.contributor.author","Hampel, Harald"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Reischies, Friedel M."],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Luckhaus, Christian"],["dc.contributor.author","Huell, Michael"],["dc.contributor.author","Gertz, Hermann-Josef"],["dc.contributor.author","Schroeder, Johannes"],["dc.contributor.author","Pantel, Johannes"],["dc.contributor.author","Rienhoff, Otto"],["dc.contributor.author","Ruether, Eckart"],["dc.contributor.author","Henn, Fritz A."],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wagner, Michael"],["dc.date.accessioned","2018-11-07T10:21:47Z"],["dc.date.available","2018-11-07T10:21:47Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: The recently proposed latent variable delta is a new tool for dementia case finding. It is built in a structural equation modeling framework of cognitive and functional data and constitutes a novel endophenotype for Alzheimer's disease (AD) research and clinical trials. Objective: To investigate the association of delta with AD biomarkers and to compare the prediction of d with established scales for conversion to dementia in patients with mild cognitive impairment (MCI). Methods: Using data from a multicenter memory clinic study, we examined the external associations of the latent variable delta and compared delta with well-established cognitive and functional scales and cognitive-functional composite scores. For that purpose, logistic regressions with cerebrospinal fluid (CSF) biomarkers and conversion to dementia as dependent variables were performed with the investigated scores. The models were tested for significant differences. Results: In patients with MCI, delta based on a broad range of cognitive scales (including the ADAS-cog, the MMSE, and the CERAD neuropsychological battery) predicted an abnormal CSF A beta(42)/tau ratio indicative of AD (n = 340, AUC = 0.78, p < 0.001), and predicted incident dementia within 1-3 years of follow-up (n = 525, AUC= 0.84, p < 0.001). These associations were generally stronger than for any other scale or cognitive-functional composite examined. Homologs of d based on reduced test batteries yielded somewhat lower effects. Conclusion: These findings support the interpretation of d as a construct capturing the disease-related \"essence\" of cognitive and functional impairments in patients with MCI and dementia, and suggest that d might become an analytical tool for dementia research."],["dc.identifier.doi","10.3233/JAD-150257"],["dc.identifier.isi","000365710600024"],["dc.identifier.pmid","26484902"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42156"],["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","The Latent Dementia Phenotype delta is Associated with Cerebrospinal Fluid Biomarkers of Alzheimer's Disease and Predicts Conversion to Dementia in Subjects with Mild Cognitive Impairment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","33"],["dc.bibliographiccitation.journal","Neurobiology of Aging"],["dc.bibliographiccitation.lastpage","40"],["dc.bibliographiccitation.volume","56"],["dc.contributor.author","Bos, Isabelle"],["dc.contributor.author","Vos, Stephanie J."],["dc.contributor.author","Frölich, Lutz"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Rüther, Eckhart"],["dc.contributor.author","Engelborghs, Sebastiaan"],["dc.contributor.author","Niemantsverdriet, Ellis"],["dc.contributor.author","De Roeck, Ellen Elisa"],["dc.contributor.author","Tsolaki, Magda"],["dc.contributor.author","Freund-Levi, Yvonne"],["dc.contributor.author","Johannsen, Peter"],["dc.contributor.author","Vandenberghe, Rik"],["dc.contributor.author","Lleó, Alberto"],["dc.contributor.author","Alcolea, Daniel"],["dc.contributor.author","Frisoni, Giovanni B."],["dc.contributor.author","Galluzzi, Samantha"],["dc.contributor.author","Nobili, Flavio"],["dc.contributor.author","Morbelli, Silvia"],["dc.contributor.author","Drzezga, Alexander"],["dc.contributor.author","Didic, Mira"],["dc.contributor.author","van Berckel, Bart N."],["dc.contributor.author","Salmon, Eric"],["dc.contributor.author","Bastin, Christine"],["dc.contributor.author","Dauby, Solene"],["dc.contributor.author","Santana, Isabel"],["dc.contributor.author","Baldeiras, Inês"],["dc.contributor.author","de Mendonça, Alexandre"],["dc.contributor.author","Silva, Dina"],["dc.contributor.author","Wallin, Anders"],["dc.contributor.author","Nordlund, Arto"],["dc.contributor.author","Coloma, Preciosa M."],["dc.contributor.author","Wientzek, Angelika"],["dc.contributor.author","Alexander, Myriam"],["dc.contributor.author","Novak, Gerald P."],["dc.contributor.author","Gordon, Mark Forrest"],["dc.contributor.author","Wallin, Åsa K."],["dc.contributor.author","Hampel, Harald"],["dc.contributor.author","Soininen, Hilkka"],["dc.contributor.author","Herukka, Sanna-Kaisa"],["dc.contributor.author","Scheltens, Philip"],["dc.contributor.author","Verhey, Frans R."],["dc.contributor.author","Visser, Pieter Jelle"],["dc.date.accessioned","2020-12-10T15:20:28Z"],["dc.date.available","2020-12-10T15:20:28Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1016/j.neurobiolaging.2017.03.034"],["dc.identifier.issn","0197-4580"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72675"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","The frequency and influence of dementia risk factors in prodromal Alzheimer's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","109"],["dc.bibliographiccitation.journal","The World Journal of Biological Psychiatry"],["dc.bibliographiccitation.lastpage","113"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Teipel, Stefan J."],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Arlt, Soenke"],["dc.contributor.author","Huell, Michael"],["dc.contributor.author","Gertz, Hermann-Josef"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Thome, Johannes"],["dc.contributor.author","Rienhoff, Otto"],["dc.contributor.author","Meindl, Thomas"],["dc.contributor.author","Hampel, Harald"],["dc.contributor.author","Grothe, Michel J."],["dc.date.accessioned","2018-11-07T08:52:32Z"],["dc.date.available","2018-11-07T08:52:32Z"],["dc.date.issued","2011"],["dc.description.abstract","Structural MRI markers may serve as surrogate endpoints in clinical trials on disease modification in Alzheimer's disease (AD). Here, we used a longitudinal MRI data set of total brain and cortical grey matter volumes from 66 patients with AD recruited across seven centres of the German Dementia Competence Network. We compared effect size estimates for the detection of a 25% reduction of atrophy progression between a priori segmentation of brain tissue, implementing an anatomical model of brain tissue distribution, and a posteriori segmentation that was not informed by an anatomical model. Additionally, we compared effect size estimates between fixed effects analysis and a mixed effects model, implementing a random effects term to account for variable spacing of observation times. A priori segmentation reduced the required sample size by 50%. Introducing a random effects term for time led to an additional 50% reduction of required samples sizes compared to fixed effects analysis. In summary, using a priori segmentation with mixed effects analysis reduced the sample size to detect clinically relevant treatment effects more than fourfold. The implementation of mixed effects models will enhance the power to detect treatment effects also with other classes of biological endpoints including molecular biomarkers of disease."],["dc.identifier.doi","10.3109/15622975.2011.603222"],["dc.identifier.isi","000294871700023"],["dc.identifier.pmid","21906007"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22192"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Informa Healthcare"],["dc.relation.issn","1562-2975"],["dc.title","Atrophy outcomes in multicentre clinical trials on Alzheimer's disease: Effect of different processing and analysis approaches on sample sizes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","7S_Part_22"],["dc.bibliographiccitation.journal","Alzheimer's & Dementia"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Bos, Isabelle"],["dc.contributor.author","Vos, Stephanie J.B."],["dc.contributor.author","Frölich, Lutz"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Rüther, Eckhart"],["dc.contributor.author","Engelborghs, Sebastiaan"],["dc.contributor.author","Niemantsverdriet, Ellis"],["dc.contributor.author","Visser, Pieter Jelle"],["dc.date.accessioned","2021-12-08T12:27:21Z"],["dc.date.available","2021-12-08T12:27:21Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1016/j.jalz.2016.06.2213"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/95324"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-476"],["dc.relation.eissn","1552-5279"],["dc.relation.issn","1552-5260"],["dc.rights.uri","http://onlinelibrary.wiley.com/termsAndConditions#vor"],["dc.title","P4‐122: Prevalence of Vascular Risk Factors in Different Stages of Prodromal Alzheimer’s Disease and Its Influence on Cognitive Decline"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","601"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neurobiology of Aging"],["dc.bibliographiccitation.lastpage","607"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Popp, Julius"],["dc.contributor.author","Wolfsgruber, Steffen"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Hüll, Michael"],["dc.contributor.author","Schröder, Johannes"],["dc.contributor.author","Möller, Hans-Jürgen"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Luckhaus, Christian"],["dc.contributor.author","Perneczky, Robert"],["dc.contributor.author","Frölich, Lutz"],["dc.contributor.author","Wagner, Michael"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Jessen, Frank"],["dc.date.accessioned","2017-09-07T11:44:32Z"],["dc.date.available","2017-09-07T11:44:32Z"],["dc.date.issued","2015"],["dc.description.abstract","Increased peripheral and central nervous system cortisol levels have been reported in Alzheimer's disease (AD) and may reflect dysfunction of cerebral components of the hypothalamic-pituitary-adrenal (HPA) axis. However, brain exposure to high cortisol concentrations may also accelerate disease progression and cognitive decline. The objectives of this study were to investigate whether HPA-axis dysregulation occurs at early clinical stages of AD and whether plasma and CSF cortisol levels are associated with clinical disease progression. Morning plasma and CSF cortisol concentrations were obtained from the subjects with AD dementia, mild cognitive impairment of AD type (MCI-AD), MCI of other type (MCI-O), and controls with normal cognition included in a multicenter study from the German Dementia Competence Network. A clinical and neuropsychological follow-up was performed in a subgroup of participants with MCI-AD, MCI-O, and AD dementia. CSF cortisol concentrations were increased in the subjects with AD dementia or MCI-AD compared with subjects with MCI-O or normal cognition. After controlling for possible confounders including CSF measures of amyloid beta1–42 and total tau, higher baseline CSF cortisol levels were associated with faster clinical worsening and cognitive decline in MCI-AD. The findings suggest that HPA-axis dysregulation occurs at the MCI stage of AD and may accelerate disease progression and cognitive decline."],["dc.identifier.doi","10.1016/j.neurobiolaging.2014.10.031"],["dc.identifier.gro","3151692"],["dc.identifier.pmid","25435336"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8511"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0197-4580"],["dc.title","Cerebrospinal fluid cortisol and clinical disease progression in MCI and dementia of Alzheimer's type"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]