Rüther, Eckart

[["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","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","6644"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Human Molecular Genetics"],["dc.bibliographiccitation.lastpage","6658"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Ramirez, Alfredo"],["dc.contributor.author","van der Flier, Wiesje M."],["dc.contributor.author","Herold, Christine"],["dc.contributor.author","Ramonet, David"],["dc.contributor.author","Heilmann, Stefanie"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Popp, Julius"],["dc.contributor.author","Lacour, André"],["dc.contributor.author","Drichel, Dmitriy"],["dc.contributor.author","Louwersheimer, Eva"],["dc.contributor.author","Kummer, Markus P."],["dc.contributor.author","Cruchaga, Carlos"],["dc.contributor.author","Hoffmann, Per"],["dc.contributor.author","Teunissen, Charlotte E."],["dc.contributor.author","Holstege, Henne"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Naj, Adam C."],["dc.contributor.author","Chouraki, Vincent"],["dc.contributor.author","Bellenguez, Céline"],["dc.contributor.author","Gerrish, Amy"],["dc.contributor.author","Heun, Reiner"],["dc.contributor.author","Frölich, Lutz"],["dc.contributor.author","Hüll, Michael"],["dc.contributor.author","Buscemi, Lara"],["dc.contributor.author","Herms, Stefan"],["dc.contributor.author","Kölsch, Heike"],["dc.contributor.author","Scheltens, Philip"],["dc.contributor.author","Breteler, Monique M."],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Goate, Alison"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Heneka, Michael T."],["dc.contributor.author","Becker, Tim"],["dc.contributor.author","Nöthen, Markus M."],["dc.date.accessioned","2017-09-07T11:44:26Z"],["dc.date.available","2017-09-07T11:44:26Z"],["dc.date.issued","2014"],["dc.description.abstract","Alzheimer’s disease (AD) is a complex disorder in which severalpathways contribute to pathology and clinical phenotype. Delineationof each pathological pathway and identification of thefactors which modulate them are crucial for the developmentof effective treatment. Information on individual pathologicalpathways is provided by biomarkers. In AD, cerebrospinalfluid (CSF) levels of Ab1–42 and phosphorylated Tau (pTau)reflect cerebral amyloid deposition and tau-related neurodegeneration,respectively. However, many of the biological factorsthat influence these core AD pathways remain elusive.Research has shown that AD risk genes contribute to CSFmarker variance (1–4). However, genes may also exist thataffect CSF markers without conferring disease susceptibility.These genes may be promising candidates for modulation ofthe disease process.The aim of the present study was to identify genetic factorsrelated to heterogeneity in pathological pathways involved inamyloid deposition and tau-related neurodegeneration—asmanifested through CSF Ab1–42 and pTau levels—and whichmight influence the clinical course of AD. To achieve this, weperformed a four-step investigation involving analysis andmeta-analysis of data from genome-wide association studies(GWASs) of these two CSF biomarkers; replication of our topfindings in an independent sample; and specific analyses andfunctional experiments to follow-up promising findings. In contrastto previous GWAS of CSF biomarkers (1,4,5), the presentGWAS was restricted to patients with dementia secondary toAD only in order to enrich for genetic effects occurring afterdisease onset."],["dc.identifier.doi","10.1093/hmg/ddu372"],["dc.identifier.gro","3151650"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8467"],["dc.language.iso","en"],["dc.notes.status","public"],["dc.notes.submitter","chake"],["dc.relation.issn","1460-2083"],["dc.title","SUCLG2 identified as both a determinator of CSF Aβ1–42 levels and an attenuator of cognitive decline in Alzheimer's disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S269"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Alzheimer s & Dementia"],["dc.bibliographiccitation.lastpage","S276"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Morgen, Katrin"],["dc.contributor.author","Ramirez, Alfredo"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Tost, Heike"],["dc.contributor.author","Plichta, Michael M."],["dc.contributor.author","Koelsch, Heike"],["dc.contributor.author","Rakebrandt, Fabian"],["dc.contributor.author","Rienhoff, Otto"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Peters, Oliver"],["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","Hampel, Harald"],["dc.contributor.author","Teipel, Stefan J."],["dc.contributor.author","Pantel, Johannes"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Ruether, Eckart"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Meyer-Lindenberg, Andreas"],["dc.date.accessioned","2018-11-07T09:34:54Z"],["dc.date.available","2018-11-07T09:34:54Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: Evidence has emerged indicating that the epsilon 4 allele of APOE and PICALM interact in conferring risk of Alzheimer's disease (AD). The biologic basis of this interaction is unclear, but it is likely to have phenotypic relevance and contribute to the structural and clinical heterogeneity of AD. Methods: The aim of this study was to investigate interaction effects of the APOE epsilon 4 allele and the alleles at the single-nucleotide polymorphism rs3851179 located in the PICALM locus. We analyzed brain volumes and cognitive phenotypes of 165 patients with early AD dementia. Results: There was a synergistic adverse effect of homozygosity for the PICALM risk allele G in rs3851179 and APOE epsilon 4 on volume in prefrontal and performance on the Trail Making Test A, which is sensitive to processing speed and working memory function. Conclusions: The data suggest a neural mechanism for APOE-PICALM interactions in patients with manifest AD and indicate that the PICALM genotype modulates both brain atrophy and cognitive performance in APOE epsilon 4 carriers. (C) 2014 The Alzheimer's Association. All rights reserved."],["dc.identifier.doi","10.1016/j.jalz.2013.11.001"],["dc.identifier.isi","000366828100002"],["dc.identifier.pmid","24613704"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32279"],["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","Genetic interaction of PICALM and APOE is associated with brain atrophy and cognitive impairment 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.firstpage","593"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Epigenomics"],["dc.bibliographiccitation.lastpage","598"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Bey, Katharina"],["dc.contributor.author","Wolfsgruber, Steffen"],["dc.contributor.author","Karaca, Ilker"],["dc.contributor.author","Wagner, Holger"],["dc.contributor.author","Lardenoije, Roy"],["dc.contributor.author","Becker, Julian"],["dc.contributor.author","Milz, Esther"],["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","Riedel-Heller, Steffi"],["dc.contributor.author","Scherer, Martin"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","van den Hove, Daniel L."],["dc.contributor.author","Rutten, Bart P. F."],["dc.contributor.author","Wagner, Michael"],["dc.contributor.author","Ramirez, Alfredo"],["dc.date.accessioned","2017-09-07T11:44:25Z"],["dc.date.available","2017-09-07T11:44:25Z"],["dc.date.issued","2016"],["dc.description.abstract","Alterations in DNA methylation have been associated with cognitive decline and Alzheimer's disease. A recent study of mild cognitive impairment (MCI) reported a significant association between annual decline in cognitive function and the rs11887120 SNP located in DNMT3A, a gene implicated in DNA methylation. Here, we aimed to replicate this finding in two independent MCI cohorts (n = 1024); however, no significant association was observed in either cohort or the pooled dataset. In stratified analyses for conversion to Alzheimer's disease status, no association between rs11887120 and cognitive decline was observed in either converters or nonconverters. In conclusion, our analyses provide no support for the hypothesis that genetic variants in DNMT3A are implicated in cognitive performance decline in individuals with MCI."],["dc.identifier.doi","10.2217/epi-2015-0014"],["dc.identifier.gro","3151644"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8460"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","1750-1911"],["dc.title","No association of the variant rs11887120 in DNMT3A with cognitive decline in individuals with mild cognitive impairment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e100812"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Wolfsgruber, Steffen"],["dc.contributor.author","Wagner, Michael"],["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","Kornhuber, Johannes"],["dc.contributor.author","Jessen, Frank"],["dc.date.accessioned","2018-11-07T09:37:42Z"],["dc.date.available","2018-11-07T09:37:42Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: Concerns about worsening memory (\"memory concerns\"; MC) and impairment in memory performance are both predictors of Alzheimer's dementia (AD). The relationship of both in dementia prediction at the pre-dementia disease stage, however, is not well explored. Refined understanding of the contribution of both MC and memory performance in dementia prediction is crucial for defining at-risk populations. We examined the risk of incident AD by MC and memory performance in patients with mild cognitive impairment (MCI). Methods: We analyzed data of 417 MCI patients from a longitudinal multicenter observational study. Patients were classified based on presence (n = 305) vs. absence (n = 112) of MC. Risk of incident AD was estimated with Cox Proportional-Hazards regression models. Results: Risk of incident AD was increased by MC (HR = 2.55, 95% CI: 1.33-4.89), lower memory performance (HR = 0.63, 95% CI: 0.56-0.71) and ApoE4-genotype (HR = 1.89, 95% CI: 1.18-3.02). An interaction effect between MC and memory performance was observed. The predictive power of MC was greatest for patients with very mild memory impairment and decreased with increasing memory impairment. Conclusions: Our data suggest that the power of MC as a predictor of future dementia at the MCI stage varies with the patients' level of cognitive impairment. While MC are predictive at early stage MCI, their predictive value at more advanced stages of MCI is reduced. This suggests that loss of insight related to AD may occur at the late stage of MCI."],["dc.identifier.doi","10.1371/journal.pone.0100812"],["dc.identifier.isi","000339618600007"],["dc.identifier.pmid","25019225"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10482"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32899"],["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","Memory Concerns, Memory Performance and Risk of Dementia in Patients with Mild Cognitive Impairment"],["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","E3"],["dc.bibliographiccitation.issue","7545"],["dc.bibliographiccitation.journal","Nature"],["dc.bibliographiccitation.lastpage","E5"],["dc.bibliographiccitation.volume","520"],["dc.contributor.author","Heilmann, Stefanie"],["dc.contributor.author","Drichel, Dmitriy"],["dc.contributor.author","Clarimon, Jordi"],["dc.contributor.author","Fernández, Victoria"],["dc.contributor.author","Lacour, André"],["dc.contributor.author","Wagner, Holger"],["dc.contributor.author","Thelen, Mathias"],["dc.contributor.author","Hernández, Isabel"],["dc.contributor.author","Fortea, Juan"],["dc.contributor.author","Alegret, Montserrat"],["dc.contributor.author","Blesa, Rafael"],["dc.contributor.author","Mauleón, Ana"],["dc.contributor.author","Roca, Maitée Rosende"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Heun, Reinhard"],["dc.contributor.author","Frölich, Lutz"],["dc.contributor.author","Hüll, Michael"],["dc.contributor.author","Heneka, Michael T."],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Riedel-Heller, Steffi"],["dc.contributor.author","Scherer, Martin"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Becker, Tim"],["dc.contributor.author","Tárraga, Lluís"],["dc.contributor.author","Boada, Mercè"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Lleó, Alberto"],["dc.contributor.author","Ruiz, Agustin"],["dc.contributor.author","Nöthen, Markus M."],["dc.contributor.author","Ramirez, Alfredo"],["dc.date.accessioned","2017-09-07T11:44:27Z"],["dc.date.available","2017-09-07T11:44:27Z"],["dc.date.issued","2015"],["dc.description.abstract","Interest in the role of rare genetic variants in the aetiology of complex diseases such as Alzheimer's disease is increasing1,2. Recently, Cruchaga et al.3 provided evidence supporting the role of rare variants in the phospholipase D3 (PLD3) gene in both familial late-onset Alzheimer's disease (age at onset >65 years) and in non-familial Alzheimer's disease. In a follow-up study of 3,568 non-familial Alzheimer's disease cases and 3,867 controls of German or Spanish descent, we failed to replicate the latter finding. Our results therefore cast doubt on the aetiological relevance of rare coding PLD3 variants in non-familial Alzheimer's disease."],["dc.identifier.doi","10.1038/nature14039"],["dc.identifier.gro","3151672"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8490"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0028-0836"],["dc.title","PLD3 in non-familial Alzheimer's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Alzheimer's Research & Therapy"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Morgen, Katrin"],["dc.contributor.author","Schneider, Michael"],["dc.contributor.author","Frölich, Lutz"],["dc.contributor.author","Tost, Heike"],["dc.contributor.author","Plichta, Michael M."],["dc.contributor.author","Kölsch, Heike"],["dc.contributor.author","Rakebrandt, Fabian"],["dc.contributor.author","Rienhoff, Otto"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Luckhaus, Christian"],["dc.contributor.author","Hüll, Michael"],["dc.contributor.author","Gertz, Hermann-Josef"],["dc.contributor.author","Schröder, Johannes"],["dc.contributor.author","Hampel, Harald"],["dc.contributor.author","Teipel, Stefan J."],["dc.contributor.author","Pantel, Johannes"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Meyer-Lindenberg, Andreas"],["dc.date.accessioned","2017-09-07T11:44:26Z"],["dc.date.available","2017-09-07T11:44:26Z"],["dc.date.issued","2015"],["dc.description.abstract","ntroductionWhite matter (WM) magnetic resonance imaging (MRI) hyperintensities are common in Alzheimer’s disease (AD), but their pathophysiological relevance and relationship to genetic factors are unclear. In the present study, we investigated potential apolipoprotein E (APOE)-dependent effects on the extent and cognitive impact of WM hyperintensities in patients with AD.MethodsWM hyperintensity volume on fluid-attenuated inversion recovery images of 201 patients with AD (128 carriers and 73 non-carriers of the APOE ε4 risk allele) was determined globally as well as regionally with voxel-based lesion mapping. Clinical, neuropsychological and MRI data were collected from prospective multicenter trials conducted by the German Dementia Competence Network.ResultsWM hyperintensity volume was significantly greater in non-carriers of the APOE ε4 allele. Lesion distribution was similar among ε4 carriers and non-carriers. Only ε4 non-carriers showed a correlation between lesion volume and cognitive performance.ConclusionThe current findings indicate an increased prevalence of WM hyperintensities in non-carriers compared with carriers of the APOE ε4 allele among patients with AD. This is consistent with a possibly more pronounced contribution of heterogeneous vascular risk factors to WM damage and cognitive impairment in patients with AD without APOE ε4-mediated risk."],["dc.identifier.doi","10.1186/s13195-015-0111-8"],["dc.identifier.gro","3151652"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8469"],["dc.language.iso","en"],["dc.notes.status","public"],["dc.notes.submitter","chake"],["dc.relation.issn","1758-9193"],["dc.title","Apolipoprotein E-dependent load of white matter hyperintensities in Alzheimer’s disease: a voxel-based lesion mapping study"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","404"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","417"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Schmidtke, Klaus"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Perneczky, Robert"],["dc.contributor.author","Wolf, Stefanie"],["dc.contributor.author","Hampel, Harald"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Weih, Markus"],["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","Seuchter, Susanne A."],["dc.contributor.author","Ruether, Eckart"],["dc.contributor.author","Henn, Fritz A."],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2018-11-07T08:34:22Z"],["dc.date.available","2018-11-07T08:34:22Z"],["dc.date.issued","2009"],["dc.description.abstract","Background: The German Dementia Competence Network (DCN) has established procedures for standardized multicenter acquisition of clinical, biological and imaging data, for centralized data management, and for the evaluation of new treatments. Methods: A longitudinal cohort study was set up for patients with mild cognitive impairment (MCI), patients with mild dementia and control subjects. The aims were to establish the diagnostic, differential diagnostic and prognostic power of a range of clinical, laboratory and imaging methods. Furthermore, 2 clinical trials were conducted with patients suffering from MCI and mild to moderate Alzheimer's Disease (AD). These trials aimed at evaluating the efficacy and safety of the combination of galantamine and memantine versus galantamine alone. Results: Here, we report on the scope and projects of the DCN, the methods that were employed, the composition and flow within the diverse groups of patients and control persons and on the clinical and neuropsychological baseline characteristics of the group of 2,113 subjects who participated in the observational and clinical trials. Conclusion: These data have an impact on the procedures for the early and differential clinical diagnosis of dementias, the current standard treatment of AD as well as on future clinical trials in AD. Copyright (C) 2009 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000210388"],["dc.identifier.isi","000266098300002"],["dc.identifier.pmid","19339779"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9317"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17792"],["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","Early and Differential Diagnosis of Dementia and Mild Cognitive Impairment Design and Cohort Baseline Characteristics of the German Dementia Competence Network"],["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","1025"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","1044"],["dc.bibliographiccitation.volume","139"],["dc.contributor.author","Kleineidam, Luca"],["dc.contributor.author","Chouraki, Vincent"],["dc.contributor.author","Próchnicki, Tomasz"],["dc.contributor.author","van der Lee, Sven J."],["dc.contributor.author","Madrid-Márquez, Laura"],["dc.contributor.author","Wagner-Thelen, Holger"],["dc.contributor.author","Karaca, Ilker"],["dc.contributor.author","Weinhold, Leonie"],["dc.contributor.author","Wolfsgruber, Steffen"],["dc.contributor.author","Boland, Anne"],["dc.contributor.author","Martino Adami, Pamela V."],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Popp, Julius"],["dc.contributor.author","Brosseron, Frederic"],["dc.contributor.author","Jansen, Iris E."],["dc.contributor.author","Hulsman, Marc"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Berr, Claudine"],["dc.contributor.author","Heun, Reinhard"],["dc.contributor.author","Frölich, Lutz"],["dc.contributor.author","Tzourio, Christophe"],["dc.contributor.author","Dartigues, Jean-François"],["dc.contributor.author","Hüll, Michael"],["dc.contributor.author","Espinosa, Ana"],["dc.contributor.author","Hernández, Isabel"],["dc.contributor.author","de Rojas, Itziar"],["dc.contributor.author","Orellana, Adelina"],["dc.contributor.author","Valero, Sergi"],["dc.contributor.author","Stringa, Najada"],["dc.contributor.author","van Schoor, Natasja M."],["dc.contributor.author","Huisman, Martijn"],["dc.contributor.author","Scheltens, Philip"],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Deleuze, Jean-Francois"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Tarraga, Lluis"],["dc.contributor.author","Schmid, Matthias"],["dc.contributor.author","Scherer, Martin"],["dc.contributor.author","Riedel-Heller, Steffi"],["dc.contributor.author","Heneka, Michael T."],["dc.contributor.author","Amouyel, Philippe"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Boada, Merce"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","González-Pérez, Antonio"],["dc.contributor.author","van der Flier, Wiesje M."],["dc.contributor.author","Wagner, Michael"],["dc.contributor.author","Lambert, Jean-Charles"],["dc.contributor.author","Holstege, Henne"],["dc.contributor.author","Sáez, Mª Eugenia"],["dc.contributor.author","Latz, Eicke"],["dc.contributor.author","Ruiz, Agustin"],["dc.contributor.author","Ramirez, Alfredo"],["dc.date.accessioned","2020-12-10T14:10:28Z"],["dc.date.available","2020-12-10T14:10:28Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1007/s00401-020-02138-6"],["dc.identifier.eissn","1432-0533"],["dc.identifier.issn","0001-6322"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70767"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","PLCG2 protective variant p.P522R modulates tau pathology and disease progression in patients with mild cognitive impairment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]