Agbemenyah, Hope Yao

[["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","32"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","EMBO molecular medicine"],["dc.bibliographiccitation.lastpage","47"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Martinez-Hernandez, Ana"],["dc.contributor.author","Urbanke, Hendrik"],["dc.contributor.author","Gillman, Alan L."],["dc.contributor.author","Lee, Joon"],["dc.contributor.author","Ryazanov, Sergey"],["dc.contributor.author","Agbemenyah, Hope Y."],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Kaurani, Lalit"],["dc.contributor.author","Grigorian, Gayane"],["dc.contributor.author","Leonov, Andrei"],["dc.contributor.author","Rezaei-Ghaleh, Nasrollah"],["dc.contributor.author","Wilken, Petra"],["dc.contributor.author","Teran Arce, Fernando"],["dc.contributor.author","Wagner, Jens"],["dc.contributor.author","Fuhrman, Martin"],["dc.contributor.author","Caruana, Mario"],["dc.contributor.author","Camilleri, Angelique"],["dc.contributor.author","Vassallo, Neville"],["dc.contributor.author","Zweckstetter, Markus"],["dc.contributor.author","Benz, Roland"],["dc.contributor.author","Giese, Armin"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Korte, Martin"],["dc.contributor.author","Lal, Ratnesh"],["dc.contributor.author","Griesinger, Christian"],["dc.contributor.author","Eichele, Gregor"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2018-01-09T14:58:18Z"],["dc.date.available","2018-01-09T14:58:18Z"],["dc.date.issued","2017-12-05"],["dc.description.abstract","Alzheimer's disease is a devastating neurodegenerative disease eventually leading to dementia. An effective treatment does not yet exist. Here we show that oral application of the compound anle138b restores hippocampal synaptic and transcriptional plasticity as well as spatial memory in a mouse model for Alzheimer's disease, when given orally before or after the onset of pathology. At the mechanistic level, we provide evidence that anle138b blocks the activity of conducting Aβ pores without changing the membrane embedded Aβ-oligomer structure. In conclusion, our data suggest that anle138b is a novel and promising compound to treat AD-related pathology that should be investigated further."],["dc.identifier.doi","10.15252/emmm.201707825"],["dc.identifier.pmid","29208638"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15064"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11613"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","1757-4684"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The diphenylpyrazole compound anle138b blocks Aβ channels and rescues disease phenotypes in a mouse model for amyloid pathology"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Tomas-Roig, J."],["dc.contributor.author","Agbemenyah, H. Y."],["dc.contributor.author","Celarain, N."],["dc.contributor.author","Quintana, E."],["dc.contributor.author","Ramió-Torrentà, Ll."],["dc.contributor.author","Havemann-Reinecke, U."],["dc.date.accessioned","2021-04-14T08:27:36Z"],["dc.date.available","2021-04-14T08:27:36Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1038/s41598-019-57290-1"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17128"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82344"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Dose-dependent effect of cannabinoid WIN-55,212-2 on myelin repair following a demyelinating insult"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","34"],["dc.bibliographiccitation.journal","Behavioural Brain Research"],["dc.bibliographiccitation.lastpage","43"],["dc.bibliographiccitation.volume","303"],["dc.contributor.author","Tomas-Roig, Jordi"],["dc.contributor.author","Piscitelli, Fabiana"],["dc.contributor.author","Gil, V."],["dc.contributor.author","del Río, José Antonio"],["dc.contributor.author","Moore, T. P."],["dc.contributor.author","Agbemenyah, Hope Yao"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Pommerenke, Claudia"],["dc.contributor.author","Lorenzen, Stephan"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.contributor.author","Di Marzo, Vincenzo"],["dc.contributor.author","Havemann-Reinecke, Ursula"],["dc.date.accessioned","2018-11-07T10:15:31Z"],["dc.date.available","2018-11-07T10:15:31Z"],["dc.date.issued","2016"],["dc.description.abstract","Prolonged and sustained stimulation of the hypothalamo pituitary adrenal axis have adverse effects on numerous brain regions, including the cerebellum. Motor coordination and motor learning are essential for animal and require the regulation of cerebellar neurons. The G-protein-coupled cannabinoid CB1 receptor coordinates synaptic transmission throughout the CNS and is of highest abundance in the cerebellum. Accordingly, the aim of this study was to investigate the long-lasting effects of chronic psychosocial stress on motor coordination and motor learning, CB1 receptor expression, endogenous cannabinoid ligands and gene expression in the cerebellum. After chronic psychosocial stress, motor coordination and motor learning were impaired as indicated the righting reflex and the rota-rod. The amount of the endocannabinoid 2-AG increased while CB1 mRNA and protein expression were downregulated after chronic stress. Transcriptome analysis revealed 319 genes differentially expressed by chronic psychosocial stress in the cerebellum; mainly involved in synaptic transmission, transmission of nerve impulse, and cell-cell signaling. Calreticulin was validated as a stress candidate gene. The present study provides evidence that chronic stress activates calreticulin and might be one of the pathological mechanisms underlying the motor coordination and motor learning dysfunctions seen in social defeat mice. (C) 2016 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.bbr.2016.01.036"],["dc.identifier.isi","000372688900005"],["dc.identifier.pmid","26815100"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40826"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1872-7549"],["dc.relation.issn","0166-4328"],["dc.title","Social defeat leads to changes in the endocannabinoid system: An overexpression of calreticulin and motor impairment in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4071"],["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","EMBO Journal"],["dc.bibliographiccitation.lastpage","4083"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Agis-Balboa, Roberto Carlos"],["dc.contributor.author","Arcos-Diaz, Dario"],["dc.contributor.author","Wittnam, Jessica"],["dc.contributor.author","Govindarajan, Nambirajan"],["dc.contributor.author","Blom, Kim"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Haladyniak, Ulla"],["dc.contributor.author","Agbemenyah, Hope Yao"],["dc.contributor.author","Zovoilis, Athanasios"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:43:23Z"],["dc.date.available","2017-09-07T11:43:23Z"],["dc.date.issued","2011"],["dc.description.abstract","Extinction learning refers to the phenomenon that a previously learned response to an environmental stimulus, for example, the expression of an aversive behaviour upon exposure to a specific context, is reduced when the stimulus is repeatedly presented in the absence of a previously paired aversive event. Extinction of fear memories has been implicated with the treatment of anxiety disease but the molecular processes that underlie fear extinction are only beginning to emerge. Here, we show that fear extinction initiates upregulation of hippocampal insulin-growth factor 2 (Igf2) and downregulation of insulin-growth factor binding protein 7 (Igfbp7). In line with this observation, we demonstrate that IGF2 facilitates fear extinction, while IGFBP7 impairs fear extinction in an IGF2-dependent manner. Furthermore, we identify one cellular substrate of altered IGF2 signalling during fear extinction. To this end, we show that fear extinctioninduced IGF2/IGFBP7 signalling promotes the survival of 17-19-day-old newborn hippocampal neurons. In conclusion, our data suggest that therapeutic strategies that enhance IGF2 signalling and adult neurogenesis might be suitable to treat disease linked to excessive fear memory."],["dc.identifier.doi","10.1038/emboj.2011.293"],["dc.identifier.gro","3142650"],["dc.identifier.isi","000295967300019"],["dc.identifier.pmid","21873981"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77"],["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","0261-4189"],["dc.title","A hippocampal insulin-growth factor 2 pathway regulates the extinction of fear memories"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4299"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","EMBO Journal"],["dc.bibliographiccitation.lastpage","4308"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Zovoilis, Athanasios"],["dc.contributor.author","Agbemenyah, Hope Yao"],["dc.contributor.author","Agis-Balboa, Roberto Carlos"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Edbauer, Dieter"],["dc.contributor.author","Rao, Pooja"],["dc.contributor.author","Farinelli, Laurent"],["dc.contributor.author","Delalle, Ivana"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Bahari-Javan, Sanaz"],["dc.contributor.author","Burkhardt, Susanne"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:43:21Z"],["dc.date.available","2017-09-07T11:43:21Z"],["dc.date.issued","2011"],["dc.description.abstract","MicroRNAs are key regulators of transcriptome plasticity and have been implicated with the pathogenesis of brain diseases. Here, we employed massive parallel sequencing and provide, at an unprecedented depth, the complete and quantitative miRNAome of the mouse hippocampus, the prime target of neurodegenerative diseases such as Alzheimer's disease (AD). Using integrative genetics, we identify miR-34c as a negative constraint of memory consolidation and show that miR-34c levels are elevated in the hippocampus of AD patients and corresponding mouse models. In line with this, targeting miR-34 seed rescues learning ability in these mouse models. Our data suggest that miR-34c could be a marker for the onset of cognitive disturbances linked to AD and indicate that targeting miR-34c could be a suitable therapy."],["dc.identifier.doi","10.1038/emboj.2011.327"],["dc.identifier.gro","3142641"],["dc.identifier.isi","000296715800017"],["dc.identifier.pmid","21946562"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/67"],["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","0261-4189"],["dc.title","MicroRNA-34c is a novel target to treat dementias"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","290"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cytogenetic and Genome Research"],["dc.bibliographiccitation.lastpage","297"],["dc.bibliographiccitation.volume","129"],["dc.contributor.author","Kifayathullah, L. A."],["dc.contributor.author","Arunachalam, J. P."],["dc.contributor.author","Bodda, Chiranjeevi"],["dc.contributor.author","Agbemenyah, H. Y."],["dc.contributor.author","Laccone, Franco A."],["dc.contributor.author","Mannan, Ashraf U."],["dc.date.accessioned","2018-11-07T08:47:29Z"],["dc.date.available","2018-11-07T08:47:29Z"],["dc.date.issued","2010"],["dc.description.abstract","The MECP2 gene, located at Xq28, encodes methyl-CpG-binding protein 2 (MeCP2), which is frequently mutated (up to 90%) in Rett syndrome (RTT). RTT is a progressive neuro-developmental disorder, which affects primarily girls during early childhood and it is one of the most common causes of mental retardation in females. R270X is one of the most frequent recurrent MECP2 mutations among RTT cohorts. The R270X mutation resides within the TRD-NLS (Transcription Repression Domain-Nuclear Localization Signal) region of MeCP2 and causes a more severe clinical phenotype with increased mortality as compared to other mutations. To evaluate the functional role of the R270X mutation, we generated a transgenic mouse model expressing MeCP2(270_EGFP) (human mutation equivalent) by BAC recombineering. The expression pattern of MeCP2(270_EGFP) was similar to that of endogenous MeCP2. Strikingly, MeCP2(270_EGFP) localizes in the nucleus, contrary to the conjecture that R270X could cause disruption of the NLS. In primary hippocampal cells, we show that MeCP2(270_EGFP) was expressed in astrocytes by colocalization with the astrocyte-specific marker glial fibrillary acidic protein. Our data showing expression of MeCP2(270_EGFP) in transgenic mice astrocytes further reinforce the recent findings concerning the expression of MeCP2 in the glial cells. Copyright (C) 2010 S. Karger AG, Basel"],["dc.description.sponsorship","DFG-Research Center for Molecular Physiology"],["dc.identifier.doi","10.1159/000315906"],["dc.identifier.isi","000280683800005"],["dc.identifier.pmid","20625242"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9102"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20963"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1424-8581"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","MeCP2(270) Mutant Protein Is Expressed in Astrocytes as well as in Neurons and Localizes in the Nucleus"],["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"]]