Rakebrandt, Fabian

[["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","244"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Psychiatry Research Neuroimaging"],["dc.bibliographiccitation.lastpage","250"],["dc.bibliographiccitation.volume","182"],["dc.contributor.author","Teipel, Stefan J."],["dc.contributor.author","Ewers, Michael"],["dc.contributor.author","Wolf, Stefanie"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Koelsch, Heike"],["dc.contributor.author","Arlt, Soenke"],["dc.contributor.author","Luckhaus, Christian"],["dc.contributor.author","Schoenknecht, Peter"],["dc.contributor.author","Schmidtke, Klaus"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Ende, Gabriele"],["dc.contributor.author","Pantel, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Rakebrandt, Fabian"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Born, Christine"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Hampel, Harald"],["dc.date.accessioned","2018-11-07T08:42:07Z"],["dc.date.available","2018-11-07T08:42:07Z"],["dc.date.issued","2010"],["dc.description.abstract","Magnetic resonance imaging (MRI)-based volumetry of medial temporal lobe regions is among the best established biomarker candidates of Alzheimer's disease (AD) to date. This study assessed the effect of multicentre variability of MRI-based hippocampus and amygdala volumetry on the discrimination between patients with Alzheimer's disease (AD) and mild cognitive impairment (MCI) and on the association of morphological changes with ApoE4 genotype and cognition. We studied 113 patients with clinically probable AD and 150 patients with amnestic MCI using high-resolution MRI scans obtained at 12 clinical sites. We determined effect sizes of group discrimination and random effects linear models, considering multicentre variability. Hippocampus and amygdala volumes were significantly reduced in AD compared with MCI patients using data pooled across centres. Multicentre variability did not significantly affect the power to detect a volume difference between AD and MCI patients. Among cognitive measures, delayed recall of verbal and non-verbal material was significantly correlated with hippocampus and amygdala volumes. Amygdala and hippocampus volumes were not associated with ApoE4 genotype in AD or MCI. Our data indicate that multicentre acquisition of MRI data using manual volumetry is reliable and feasible for cross-sectional diagnostic studies, and they replicate essential findings from smaller scale monocentre studies. (C) 2010 Published by Elsevier Ireland Ltd."],["dc.description.sponsorship","Bundesministeriums fur Bildung und Forschung (BMBF) [01 GI 0102]"],["dc.identifier.doi","10.1016/j.pscychresns.2010.03.003"],["dc.identifier.isi","000279521300009"],["dc.identifier.pmid","20493672"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19635"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","0925-4927"],["dc.title","Multicentre variability of MRI-based medial temporal lobe volumetry 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.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","389"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Alzheimer s Disease"],["dc.bibliographiccitation.lastpage","401"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Morgen, Katrin"],["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","2018-11-07T09:29:40Z"],["dc.date.available","2018-11-07T09:29:40Z"],["dc.date.issued","2013"],["dc.description.abstract","Background: The E4 isoform of the APOE genotype is the most significant genetic risk factor for sporadic Alzheimer's disease (AD) and has recently been found to modulate disease expression in patients with AD. Objective: To investigate APOE-dependent cognitive and structural phenotypes in subjects with mild cognitive impairment who converted to AD within the following three years. Methods: Subjects converting to AD (n = 63) were compared to a control group with stable mild cognitive impairment (n = 131). Clinical, neuropsychological, and MRI data were obtained by the German Dementia Competence Network. Subgroups of converting and stable APOE E4 carriers and non-carriers were investigated longitudinally with MRI to examine structural correlates of conversion. Voxel-based morphometry was applied to investigate gray matter distribution. Results: At baseline, executive performance correlated with global and bilateral prefrontal gray matter volume and predicted conversion only among non-carriers. Converting carriers and non-carriers presented distinct patterns of brain atrophy on longitudinal analysis, in line with a dissociation between more pronounced occipital atrophy in carriers and more frontoparietal volume loss in non-carriers at follow-up. Conclusions: The current findings suggest that in APOE E4 non-carriers with AD, executive dysfunction is closely linked to frontal gray matter atrophy and predictive of progression to dementia. The results are consistent with APOE genotype-dependent profiles of structural damage and cognitive decline in patients with imminent conversion to AD."],["dc.identifier.doi","10.3233/JAD-130326"],["dc.identifier.isi","000324338400013"],["dc.identifier.pmid","23948881"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31097"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ios Press"],["dc.relation.issn","1387-2877"],["dc.title","APOE-Dependent Phenotypes in Subjects with Mild Cognitive Impairment Converting to Alzheimer's Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]