Fischer, André

[["dc.bibliographiccitation.firstpage","135"],["dc.bibliographiccitation.journal","Neurobiology of Disease"],["dc.bibliographiccitation.lastpage","143"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Agbemenyah, Hope Yao"],["dc.contributor.author","Agis-Balboa, Roberto Carlos"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Delalle, Ivana"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:46:53Z"],["dc.date.available","2017-09-07T11:46:53Z"],["dc.date.issued","2014"],["dc.description.abstract","Alzheimer's disease (AD) is the most common form of dementia in the elderly but effective therapeutic strategies to treat AD are not yet available. This is also due to the fact that the pathological mechanisms that drive the pathogenesis of sporadic AD are still not sufficiently understood and may differ on the individual level. Several risk factors such as altered insulin-like peptide (ILP) signaling have been linked to AD and modulating the ILP system has been discussed as a potential therapeutic avenue. Here we show that insulin-like growth factor binding protein 7 (IGFBP7), a protein that attenuates the function of ILPs, is up-regulated in the brains of AD patients and in a mouse model for AD via a process that involves altered DNA-methylation and coincides with decreased ILP signaling. Mimicking the AD-situation in wild type mice, by increasing hippocampal IGFBP7 levels leads to impaired memory consolidation. Consistently, inhibiting IGFBP7 function in mice that develop AD-like memory impairment reinstates associative learning behavior. These data suggest that IGFBP7 is a critical regulator of memory consolidation and might be used as a biomarker for AD. Targeting IGFBP7 could be a novel therapeutic avenue for the treatment of AD patients."],["dc.identifier.doi","10.1016/j.nbd.2013.09.011"],["dc.identifier.gro","3142193"],["dc.identifier.isi","000330553600013"],["dc.identifier.pmid","24075854"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5566"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1095-953X"],["dc.relation.issn","0969-9961"],["dc.title","Insulin growth factor binding protein 7 is a novel target to treat dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2815"],["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","The EMBO journal"],["dc.bibliographiccitation.lastpage","2828"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Agis-Balboa, Roberto Carlos"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Pinheiro, Paulo S."],["dc.contributor.author","Rebola, Nelson"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Gertig, Michael"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Delalle, Ivana"],["dc.contributor.author","Jatzko, Alexander"],["dc.contributor.author","Dettenhofer, Markus"],["dc.contributor.author","Zunszain, Patricia A"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Pape, Julius C"],["dc.contributor.author","Binder, Elisabeth B."],["dc.contributor.author","Mulle, Christophe"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.date.accessioned","2018-01-09T14:50:41Z"],["dc.date.available","2018-01-09T14:50:41Z"],["dc.date.issued","2017"],["dc.description.abstract","Age-associated memory decline is due to variable combinations of genetic and environmental risk factors. How these risk factors interact to drive disease onset is currently unknown. Here we begin to elucidate the mechanisms by which post-traumatic stress disorder (PTSD) at a young age contributes to an increased risk to develop dementia at old age. We show that the actin nucleator Formin 2 (Fmn2) is deregulated in PTSD and in Alzheimer's disease (AD) patients. Young mice lacking the Fmn2 gene exhibit PTSD-like phenotypes and corresponding impairments of synaptic plasticity, while the consolidation of new memories is unaffected. However, Fmn2 mutant mice develop accelerated age-associated memory decline that is further increased in the presence of additional risk factors and is mechanistically linked to a loss of transcriptional homeostasis. In conclusion, our data present a new approach to explore the connection between AD risk factors across life span and provide mechanistic insight to the processes by which neuropsychiatric diseases at a young age affect the risk for developing dementia."],["dc.identifier.doi","10.15252/embj.201796821"],["dc.identifier.pmid","28768717"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14923"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11608"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","1460-2075"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Formin 2 links neuropsychiatric phenotypes at young age to an increased risk for dementia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.contributor.author","Fischer, André"],["dc.contributor.author","Sakib, M Sadman"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Schütz, Anna-Lena"],["dc.contributor.author","Irniger, Stefan"],["dc.contributor.author","Capece, Vincenzo"],["dc.date.accessioned","2018-04-11T16:20:54Z"],["dc.date.available","2018-04-11T16:20:54Z"],["dc.date.issued","2016"],["dc.description.abstract","Although histone modifications and DNA methylation have been meticulously studied in the context of learning & memory formation, very few studies have demonstrated non-canonical histone variants as potential regulators of memory formation. Compared to canonical histones, these histone variants are expressed independently of DNA replication and are important for many physiological events as they confer altered chromatin structures, thereby regulating transcription. Recently, H2A.Z (variant of canonical histone, H2A) has been reported as a novel epigenetic regulator in memory formation (Zovkic et. al. 2014), which raised the question, whether differential binding of H2A.Z or its modification (e.g acetylation) across the whole genome could be a stable modulator for life-long memory acquisition and cognition. Here, we investigated genomic regions bound by H2A.Z and its acetylated variant (H2A.Zac) using chromatin immunoprecipitation followed by sequencing (ChIP-seq) in FACS-sorted neuronal and nonneuronal nuclei from hippocampal CA1 region. Initially, mRNA levels of H2afz (gene of H2A.Z) were assessed in CA1 region of aged (16 months old) and Alzheimer’s model mice (5XFAD) comparing them to young (3 months old) and wild type mice respectively. Furthermore, ChIP protocols for H2A.Z and H2A.Zac were optimized, as it has not been done before in this context. As a model of enhanced cognition, hippocampal CA1 regions from mice subjected to 4 months enriched environment (EE) were used for ChIP-seq against H2A.Z and H2A.Zac, comparing to home caged animals as controls. ChIP-seq analysis showed decreased binding of H2A.Z and its de-acetylation at specific promoter regions in CA1 neurons upon environmental enrichment. Promoters with decreased binding or decreased acetylation were found to be involved in genes functionally associated with neurogenesis, synaptic plasticity and several biosynthetic pathways. Further study is needed to prove their effect on transcription of those genes."],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13225"],["dc.language.iso","en"],["dc.notes.preprint","yes"],["dc.notes.status","final"],["dc.relation.eventend","4"],["dc.relation.eventlocation","Obergurgl, Austria"],["dc.relation.eventstart","28"],["dc.relation.iserratumof","yes"],["dc.title","Differential binding of non-canonical histone variant H2A.Z & its de-acetylation is evident in enhanced cognitive function"],["dc.type","conference_paper"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3452"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","The Journal of neuroscience"],["dc.bibliographiccitation.lastpage","3464"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Agis-Balboa, Roberto Carlos"],["dc.contributor.author","Kranz, Andrea"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Halder, Rashi"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Stewart, Adrian Francis"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:47:49Z"],["dc.date.available","2017-09-07T11:47:49Z"],["dc.date.issued","2013"],["dc.description.abstract","The consolidation of long-term memories requires differential gene expression. Recent research has suggested that dynamic changes in chromatin structure play a role in regulating the gene expression program linked to memory formation. The contribution of histone methylation, an important regulatory mechanism of chromatin plasticity that is mediated by the counteracting activity of histone-methyltransferases and histone-demethylases, is, however, not well understood. Here we show that mice lacking the histone-methyltransferase myeloid/lymphoid or mixed-lineage leukemia 2 (mll2/kmt2b) gene in adult forebrain excitatory neurons display impaired hippocampus-dependent memory function. Consistent with the role of KMT2B in gene-activation DNA microarray analysis revealed that 152 genes were downregulated in the hippocampal dentate gyrus region of mice lacking kmt2b. Downregulated plasticity genes showed a specific deficit in histone 3 lysine 4 di-and trimethylation, while histone 3 lysine 4 monomethylation was not affected. Our data demonstrates that KMT2B mediates hippocampal histone 3 lysine 4 di-and trimethylation and is a critical player for memory formation."],["dc.identifier.doi","10.1523/JNEUROSCI.3356-12.2013"],["dc.identifier.gro","3142390"],["dc.identifier.isi","000315195700021"],["dc.identifier.pmid","23426673"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7752"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0270-6474"],["dc.title","Histone-Methyltransferase MLL2 (KMT2B) Is Required for Memory Formation in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","753"],["dc.bibliographiccitation.issue","5979"],["dc.bibliographiccitation.journal","Science"],["dc.bibliographiccitation.lastpage","756"],["dc.bibliographiccitation.volume","328"],["dc.contributor.author","Peleg, Shahaf"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Zovoilis, Athanasios"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Agis-Balboa, Roberto Carlos"],["dc.contributor.author","Cota, Perla"],["dc.contributor.author","Wittnam, Jessica"],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Dettenhofer, Markus"],["dc.contributor.author","Kang, Hui"],["dc.contributor.author","Farinelli, Laurent"],["dc.contributor.author","Chen, Wei"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Doering, Aaron"],["dc.date.accessioned","2017-09-07T11:46:04Z"],["dc.date.available","2017-09-07T11:46:04Z"],["dc.date.issued","2010"],["dc.description.abstract","As the human life span increases, the number of people suffering from cognitive decline is rising dramatically. The mechanisms underlying age-associated memory impairment are, however, not understood. Here we show that memory disturbances in the aging brain of the mouse are associated with altered hippocampal chromatin plasticity. During learning, aged mice display a specific deregulation of histone H4 lysine 12 (H4K12) acetylation and fail to initiate a hippocampal gene expression program associated with memory consolidation. Restoration of physiological H4K12 acetylation reinstates the expression of learning-induced genes and leads to the recovery of cognitive abilities. Our data suggest that deregulated H4K12 acetylation may represent an early biomarker of an impaired genome-environment interaction in the aging mouse brain."],["dc.identifier.doi","10.1126/science.1186088"],["dc.identifier.gro","3142928"],["dc.identifier.isi","000277357100040"],["dc.identifier.pmid","20448184"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/386"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0036-8075"],["dc.title","Altered Histone Acetylation Is Associated with Age-Dependent Memory Impairment in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5062"],["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","5073"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Maddalena, Andrea"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Wittnam, Jessica"],["dc.contributor.author","Held, Torsten"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Delalle, Ivanna"],["dc.contributor.author","Kügler, Sebastian"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.date.accessioned","2017-09-07T11:48:54Z"],["dc.date.available","2017-09-07T11:48:54Z"],["dc.date.issued","2012"],["dc.description.abstract","Histone acetylation has been implicated with the pathogenesis of neuropsychiatric disorders and targeting histone deacetylases (HDACs) using HDAC inhibitors was shown to be neuroprotective and to initiate neuroregenerative processes. However, little is known about the role of individual HDAC proteins during the pathogenesis of brain diseases. HDAC1 was found to be upregulated in patients suffering from neuropsychiatric diseases. Here, we show that virus-mediated overexpression of neuronal HDAC1 in the adult mouse hippocampus specifically affects the extinction of contextual fear memories, while other cognitive abilities were unaffected. In subsequent experiments we show that under physiological conditions, hippocampal HDAC1 is required for extinction learning via a mechanism that involves H3K9 deacetylation and subsequent trimethylation of target genes. In conclusion, our data show that hippocampal HDAC1 has a specific role in memory function."],["dc.identifier.doi","10.1523/JNEUROSCI.0079-12.2012"],["dc.identifier.gro","3142550"],["dc.identifier.isi","000302793500005"],["dc.identifier.pmid","22496552"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8456"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8913"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0270-6474"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","HDAC1 Regulates Fear Extinction in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3572"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.lastpage","3584"],["dc.bibliographiccitation.volume","125"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Urbanke, Hendrik"],["dc.contributor.author","Ramachandran, Binu"],["dc.contributor.author","Barth, Jonas"],["dc.contributor.author","Haider, Rashi"],["dc.contributor.author","Awasthi, Ankit"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Navarro-Sala, Magdalena"],["dc.contributor.author","Nagarajan, Sankari"],["dc.contributor.author","Schuetz, Anna-Lena"],["dc.contributor.author","Johnsen, Steven A."],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Luehrmann, Reinhard"],["dc.contributor.author","Dean, Camin"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:43:34Z"],["dc.date.available","2017-09-07T11:43:34Z"],["dc.date.issued","2015"],["dc.description.abstract","Aging and increased amyloid burden are major risk factors for cognitive diseases such as Alzheimer's disease (AD). Effective therapies for these diseases are lacking. Here, we evaluated mouse models of age-associated memory impairment and amyloid deposition to study transcriptome and cell type-specific epigenome plasticity in the brain and peripheral organs. We determined that aging and amyloid pathology are associated with inflammation and impaired synaptic function in the hippocampal CA1 region as the result of epigenetic-dependent alterations in gene expression. In both amyloid and aging models, inflammation was associated with increased gene expression linked to a subset of transcription factors, while plasticity gene deregulation was differentially mediated. Amyloid pathology impaired histone acetylation and decreased expression of plasticity genes, while aging altered H4K12 acetylation-linked differential splicing at the intron-exon junction in neurons, but not nonneuronal cells. Furthermore, oral administration of the clinically approved histone deacetylase inhibitor vorinostat not only restored spatial memory, but also exerted antiinflammatory action and reinstated epigenetic balance and transcriptional homeostasis at the level of gene expression and exon usage. This study provides a systems-level investigation of transcriptome plasticity in the hippocampal CA1 region in aging and AD models and suggests that histone deacetylase inhibitors should be further explored as a cost-effective therapeutic strategy against age-associated cognitive decline."],["dc.identifier.doi","10.1172/JCI79942"],["dc.identifier.gro","3141833"],["dc.identifier.isi","000362303600031"],["dc.identifier.pmid","26280576"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1579"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1558-8238"],["dc.relation.issn","0021-9738"],["dc.title","HDAC inhibitor-dependent transcriptome and memory reinstatement in cognitive decline models"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.volume","13"],["dc.contributor.affiliation","Islam, Md Rezaul; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Kaurani, Lalit; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Berulava, Tea; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Heilbronner, Urs; 3Institute of Psychiatric Phenomics and Genomics (IPPG), University Hospital Ludwig‐Maximilians‐University Munich Munich Germany"],["dc.contributor.affiliation","Budde, Monika; 3Institute of Psychiatric Phenomics and Genomics (IPPG), University Hospital Ludwig‐Maximilians‐University Munich Munich Germany"],["dc.contributor.affiliation","Centeno, Tonatiuh Pena; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Elerdashvili, Vakthang; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Zafieriou, Maria‐Patapia; 4Institute of Pharmacology and Toxicology University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Benito, Eva; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Sertel, Sinem M; 5Department of Neuro‐ and Sensory Physiology University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Goldberg, Maria; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Senner, Fanny; 3Institute of Psychiatric Phenomics and Genomics (IPPG), University Hospital Ludwig‐Maximilians‐University Munich Munich Germany"],["dc.contributor.affiliation","Kalman, Janos L; 3Institute of Psychiatric Phenomics and Genomics (IPPG), University Hospital Ludwig‐Maximilians‐University Munich Munich Germany"],["dc.contributor.affiliation","Burkhardt, Susanne; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Oepen, Anne Sophie; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Sakib, Mohammad Sadman; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Kerimoglu, Cemil; 1Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases German Center for Neurodegenerative Diseases Göttingen Germany"],["dc.contributor.affiliation","Wirths, Oliver; 2Department for Psychiatry and Psychotherapy University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Bickeböller, Heike; 7Department of Genetic Epidemiology University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Bartels, Claudia; 2Department for Psychiatry and Psychotherapy University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Brosseron, Frederic; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Buerger, Katharina; 10German Center for Neurodegenerative Diseases (DZNE, Munich) Munich Germany"],["dc.contributor.affiliation","Cosma, Nicoleta‐Carmen; 12Department of Psychiatry and Psychotherapy Charité – Universitätsmedizin Berlin Berlin Germany"],["dc.contributor.affiliation","Fliessbach, Klaus; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Heneka, Michael T.; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Janowitz, Daniel; 11Institute for Stroke and Dementia Research (ISD) University Hospital LMU Munich Munich Germany"],["dc.contributor.affiliation","Kilimann, Ingo; 13German Center for Neurodegenerative Diseases (DZNE) Rostock Germany"],["dc.contributor.affiliation","Kleinedam, Luca; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Laske, Christoph; 14Department of Psychosomatic Medicine Rostock University Medical Center Rostock Germany"],["dc.contributor.affiliation","Metzger, Coraline D; 16German Center for Neurodegenerative Diseases (DZNE) Magdeburg Germany"],["dc.contributor.affiliation","Munk, Matthias H; 15Section for Dementia Research Hertie Institute for Clinical Brain Research and Department of Psychiatry and Psychotherapy University of Tübingen Tübingen Germany"],["dc.contributor.affiliation","Perneczky, Robert; 6Department of Psychiatry and Psychotherapy Ludwig‐Maximilians‐University Munich München Germany"],["dc.contributor.affiliation","Peters, Oliver; 12Department of Psychiatry and Psychotherapy Charité – Universitätsmedizin Berlin Berlin Germany"],["dc.contributor.affiliation","Priller, Josef; 22German Center for Neurodegenerative Diseases (DZNE) Berlin Germany"],["dc.contributor.affiliation","Rauchmann, Boris S.; 6Department of Psychiatry and Psychotherapy Ludwig‐Maximilians‐University Munich München Germany"],["dc.contributor.affiliation","Roy, Nina; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Schneider, Anja; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Spottke, Annika; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Spruth, Eike J; 22German Center for Neurodegenerative Diseases (DZNE) Berlin Germany"],["dc.contributor.affiliation","Teipel, Stefan; 13German Center for Neurodegenerative Diseases (DZNE) Rostock Germany"],["dc.contributor.affiliation","Tscheuschler, Maike; 25Department of Psychiatry Medical Faculty University of Cologne Cologne Germany"],["dc.contributor.affiliation","Wagner, Michael; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Wiltfang, Jens; 2Department for Psychiatry and Psychotherapy University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Düzel, Emrah; 16German Center for Neurodegenerative Diseases (DZNE) Magdeburg Germany"],["dc.contributor.affiliation","Jessen, Frank; 8German Center for Neurodegenerative Diseases Bonn Germany"],["dc.contributor.affiliation","Rizzoli, Silvio O; 5Department of Neuro‐ and Sensory Physiology University Medical Center Göttingen Göttingen Germany"],["dc.contributor.affiliation","Zimmermann, Wolfram‐Hubertus; 4Institute of Pharmacology and Toxicology University Medical Center Göttingen Göttingen Germany"],["dc.contributor.author","Islam, Md Rezaul"],["dc.contributor.author","Kaurani, Lalit"],["dc.contributor.author","Berulava, Tea"],["dc.contributor.author","Heilbronner, Urs"],["dc.contributor.author","Budde, Monika"],["dc.contributor.author","Centeno, Tonatiuh Pena"],["dc.contributor.author","Elerdashvili, Vakthang"],["dc.contributor.author","Zafieriou, Maria‐Patapia"],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Sertel, Sinem M."],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Rizzoli, Silvio O."],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Schulze, Thomas G."],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.authorgroup","Delcode Study Group"],["dc.date.accessioned","2021-12-01T09:24:01Z"],["dc.date.available","2021-12-01T09:24:01Z"],["dc.date.issued","2021"],["dc.date.updated","2022-03-21T13:34:49Z"],["dc.description.abstract","Abstract While some individuals age without pathological memory impairments, others develop age‐associated cognitive diseases. Since changes in cognitive function develop slowly over time in these patients, they are often diagnosed at an advanced stage of molecular pathology, a time point when causative treatments fail. Thus, there is great need for the identification of inexpensive and minimal invasive approaches that could be used for screening with the aim to identify individuals at risk for cognitive decline that can then undergo further diagnostics and eventually stratified therapies. In this study, we use an integrative approach combining the analysis of human data and mechanistic studies in model systems to identify a circulating 3‐microRNA signature that reflects key processes linked to neural homeostasis and inform about cognitive status. We furthermore provide evidence that expression changes in this signature represent multiple mechanisms deregulated in the aging and diseased brain and are a suitable target for RNA therapeutics."],["dc.description.abstract","SYNOPSIS image Alzheimer\\’s disease (AD) is usually diagnosed at an advanced stage of molecular pathology, a time point when causative treatments fail. This study aimed to identify a minimally invasive biomarker that can help to identify individuals at risk for cognitive decline before clinical manifestation. Circulating microRNAs are linked to cognitive function in young and healthy humans. A circulating 3‐microRNA signature is identified using a longitudinal mouse model of age‐associated memory decline. The expression of the 3‐microRNA signature is increased in patients with mild cognitive impairment (MCI) and is associated with future conversion from MCI to AD. Targeting all 3‐ microRNAs using anti‐miRs ameliorates cognitive decline in AD mice."],["dc.description.abstract","Alzheimer\\’s disease (AD) is usually diagnosed at an advanced stage of molecular pathology, a time point when causative treatments fail. This study aimed to identify a minimally invasive biomarker that can help to identify individuals at risk for cognitive decline before clinical manifestation. image"],["dc.description.sponsorship","EC|H2020|H2020 Priority Excellent Science|H2020 European Research Council (ERC) http://dx.doi.org/10.13039/100010663"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft (DFG) http://dx.doi.org/10.13039/501100001659"],["dc.description.sponsorship","Bundesministerium für Bildung und Forschung (BMBF) http://dx.doi.org/10.13039/501100002347"],["dc.description.sponsorship","HHS|NIH|OSC|Common Fund (NIH Common Fund) http://dx.doi.org/10.13039/100015326"],["dc.identifier.doi","10.15252/emmm.202013659"],["dc.identifier.pmid","34633146"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94824"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/411"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/150"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | B06: Die Rolle von RNA in Synapsenphysiologie und Neurodegeneration"],["dc.relation.eissn","1757-4684"],["dc.relation.issn","1757-4676"],["dc.relation.workinggroup","RG A. Fischer (Epigenetics and Systems Medicine in Neurodegenerative Diseases)"],["dc.relation.workinggroup","RG Zafeiriou (3D Electrically Excitable Cell Networks – Brain and Heart)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited."],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","A microRNA signature that correlates with cognition and is a target against cognitive decline"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","2149"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific reports"],["dc.bibliographiccitation.lastpage","19"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Burk, Katja"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Murdoch, John D"],["dc.contributor.author","Koenig, Melanie"],["dc.contributor.author","Bharat, Vinita"],["dc.contributor.author","Markworth, Ronja"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Dean, Camin"],["dc.date.accessioned","2018-01-09T14:36:50Z"],["dc.date.available","2018-01-09T14:36:50Z"],["dc.date.issued","2017-05-19"],["dc.description.abstract","The sorting of activated receptors into distinct endosomal compartments is essential to activate specific signaling cascades and cellular events including growth and survival. However, the proteins involved in this sorting are not well understood. We discovered a novel role of EndophilinAs in sorting of activated BDNF-TrkB receptors into late endosomal compartments. Mice lacking all three EndophilinAs accumulate Rab7-positive late endosomes. Moreover, EndophilinAs are differentially localized to, co-traffic with, and tubulate, distinct endosomal compartments: In response to BDNF, EndophilinA2 is recruited to both early and late endosomes, EndophilinA3 is recruited to Lamp1-positive late endosomes, and co-trafficks with Rab5 and Rab7 in both the presence and absence of BDNF, while EndophilinA1 colocalizes at lower levels with endosomes. The absence of all three EndophilinAs caused TrkB to accumulate in EEA1 and Rab7-positive endosomes, and impaired BDNF-TrkB-dependent survival signaling cascades. In addition, EndophilinA triple knockout neurons exhibited increased cell death which could not be rescued by exogenous BDNF, in a neurotrophin-dependent survival assay. Thus, EndophilinAs differentially regulate activated receptor sorting via distinct endosomal compartments to promote BDNF-dependent cell survival."],["dc.identifier.doi","10.1038/s41598-017-02202-4"],["dc.identifier.pmid","28526875"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14709"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11603"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","EndophilinAs regulate endosomal sorting of BDNF-TrkB to mediate survival signaling in hippocampal neurons"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","538"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.lastpage","548"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Sakib, M Sadman"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Capece, Vincenzo"],["dc.contributor.author","Kaurani, Lalit"],["dc.contributor.author","Halder, Rashi"],["dc.contributor.author","Agis-Balboa, Roberto Carlos"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Urbanke, Hendrik"],["dc.contributor.author","Kranz, Andrea"],["dc.contributor.author","Stewart, Adrian Francis"],["dc.date.accessioned","2018-01-09T14:45:29Z"],["dc.date.available","2018-01-09T14:45:29Z"],["dc.date.issued","2017-07-18"],["dc.description.abstract","Kmt2a and Kmt2b are H3K4 methyltransferases of the Set1/Trithorax class. We have recently shown the importance of Kmt2b for learning and memory. Here, we report that Kmt2a is also important in memory formation. We compare the decrease in H3K4 methylation and de-regulation of gene expression in hippocampal neurons of mice with knockdown of either Kmt2a or Kmt2b. Kmt2a and Kmt2b control largely distinct genomic regions and different molecular pathways linked to neuronal plasticity. Finally, we show that the decrease in H3K4 methylation resulting from Kmt2a knockdown partially recapitulates the pattern previously reported in CK-p25 mice, a model for neurodegeneration and memory impairment. Our findings point to the distinct functions of even closely related histone-modifying enzymes and provide essential insight for the development of more efficient and specific epigenetic therapies against brain diseases."],["dc.identifier.doi","10.1016/j.celrep.2017.06.072"],["dc.identifier.pmid","28723559"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11606"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","2211-1247"],["dc.title","KMT2A and KMT2B Mediate Memory Function by Affecting Distinct Genomic Regions"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]