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","786"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","798"],["dc.bibliographiccitation.volume","55"],["dc.contributor.author","Schrick, Christina"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Srivastava, Deepak P."],["dc.contributor.author","Tronson, Natalie C."],["dc.contributor.author","Penzes, Peter"],["dc.contributor.author","Radulovic, Jelena"],["dc.date.accessioned","2017-09-07T11:49:25Z"],["dc.date.available","2017-09-07T11:49:25Z"],["dc.date.issued","2007"],["dc.description.abstract","Cadherin-mediated interactions are integral to synapse formation and potentiation. Here we show that N-cadherin is required for memory formation and regulation of a subset of underlying biochemical processes. N-cadherin antagonistic peptide containing the His-Ala-Val motif (HAV-N) transiently disrupted hippocampal N-cadherin dimerization and impaired the formation of long-term contextual fear memory while sparing short-term memory, retrieval, and extinction. HAV-N impaired the learning-induced phosphorylation of a distinctive, cytoskeletally associated fraction of hippocampal Erk-1/2 and altered the distribution of IQGAP1, a scaffold protein linking cadherin-mediated cell adhesion to the cytoskeleton. This effect was accompanied by reduction of N-cadherin/ IQGAP1/Erk-2 interactions. Similarly, in primary neuronal cultures, HAV-N prevented NMDA-induced dendritic Erk-1/2 phosphorylation and caused relocation of IQGAP1 from dendritic spines into the shafts. The data suggest that the newly identified role of hippocampal N-cadherin in memory consolidation may be mediated, at least in part, by cytoskeletal IQGAP1/Erk signaling."],["dc.identifier.doi","10.1016/j.neuron.2007.07.034"],["dc.identifier.gro","3143441"],["dc.identifier.isi","000249857000014"],["dc.identifier.pmid","17785185"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/955"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: NIMH NIH HHS [R01 MH073669, R01 MH073669-02]"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0896-6273"],["dc.title","N-cadherin regulates cytoskeletally associated lQGAP1/ERK signaling and memory formation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1145"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Biological Chemistry"],["dc.bibliographiccitation.lastpage","1153"],["dc.bibliographiccitation.volume","390"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:46:46Z"],["dc.date.available","2017-09-07T11:46:46Z"],["dc.date.issued","2009"],["dc.description.abstract","The orchestrated expression of genes is essential for the development and survival of every organism. In addition to the role of transcription factors, the availability of genes for transcription is controlled by a series of proteins that regulate epigenetic chromatin remodeling. The two most studied epigenetic phenomena are DNA methylation and histone-tail modifications. Although a large body of literature implicates the deregulation of histone acetylation and DNA methylation with the pathogenesis of cancer, recently epigenetic mechanisms have also gained much attention in the neuroscientific community. In fact, a new field of research is rapidly emerging and there is now accumulating evidence that the molecular machinery that regulates histone acetylation and DNA methylation is intimately involved in synaptic plasticity and is essential for learning and memory. Importantly, dysfunction of epigenetic gene expression in the brain might be involved in neurodegenerative and psychiatric diseases. In particular, it was found that inhibition of histone deacetylases attenuates synaptic and neuronal loss in animal models for various neurodegenerative diseases and improves cognitive function. In this article, we will summarize recent data in the novel field of neuroepigenetics and discuss the question why epigenetic strategies are suitable therapeutic approaches for the treatment of brain diseases."],["dc.identifier.doi","10.1515/BC.2009.131"],["dc.identifier.gro","3143028"],["dc.identifier.isi","000270513600009"],["dc.identifier.pmid","19747081"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/497"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: European Science Foundation"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1431-6730"],["dc.title","The epigenetic bottleneck of neurodegenerative and psychiatric diseases"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Current Neurology and Neuroscience Reports"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Zarranz, Juan-José"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Ferrer, Isidro"],["dc.date.accessioned","2018-04-23T11:47:17Z"],["dc.date.available","2018-04-23T11:47:17Z"],["dc.date.issued","2017"],["dc.description.abstract","Purpose of Review Fatal familiar insomnia (FFI) is an autosomal dominant inherited prion disease caused by D178N mutation in the prion protein gene (PRNP D178N) accompanied by the presence of a methionine at the codon 129 polymorphic site on the mutated allele. FFI is characterized by severe sleep disorder, dysautonomia, motor signs and abnormal behaviour together with primary atrophy of selected thalamic nuclei and inferior olives, and expansion to other brain regions with disease progression. This article reviews recent research on the clinical and molecular aspects of the disease. Recent Findings New clinical and biomarker tools have been implemented in order to assist in the diagnosis of the disease. In addition, the generation of mouse models, the availability of ‘omics’ data in brain tissue and the use of new seeding techniques shed light on the molecular events in FFI pathogenesis. Biochemical studies in human samples also reveal that neuropathological alterations in vulnerable brain regions underlie severe impairment in key cellular processes such as mitochondrial and protein synthesis machinery. Summary Although the development of a therapy is still a major challenge, recent findings represent a step toward understanding of the clinical and molecular aspects of FFI."],["dc.identifier.doi","10.1007/s11910-017-0743-0"],["dc.identifier.gro","3142200"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13320"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","1528-4042"],["dc.title","Fatal Familial Insomnia: Clinical Aspects and Molecular Alterations"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Cell and Developmental Biology"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Abbas, Eman"],["dc.contributor.author","Hassan, Mohamed A."],["dc.contributor.author","Sokpor, Godwin"],["dc.contributor.author","Kiszka, Kamila"],["dc.contributor.author","Pham, Linh"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Nguyen, Huu Phuc"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2021-09-01T06:38:19Z"],["dc.date.available","2021-09-01T06:38:19Z"],["dc.date.issued","2021"],["dc.description.abstract","Oligodendrocytes are responsible for axon myelination in the brain and spinal cord. Generation of oligodendrocytes entails highly regulated multistage neurodevelopmental events, including proliferation, differentiation and maturation. The chromatin remodeling BAF (mSWI/SNF) complex is a notable regulator of neural development. In our previous studies, we determined the indispensability of the BAF complex scaffolding subunits BAF155 and BAF170 for neurogenesis, whereas their role in gliogenesis is unknown. Here, we show that the expression of BAF155 and BAF170 is essential for the genesis of oligodendrocytes during brain development. We report that the ablation of BAF155 and BAF170 in the dorsal telencephalic (dTel) neural progenitors or in oligodendrocyte-producing progenitors in the ventral telencephalon (vTel) in double-conditional knockout (dcKO) mouse mutants, perturbed the process of oligodendrogenesis. Molecular marker and cell cycle analyses revealed impairment of oligodendrocyte precursor specification and proliferation, as well as overt depletion of oligodendrocytes pool in dcKO mutants. Our findings unveil a central role of BAF155 and BAF170 in oligodendrogenesis, and thus substantiate the involvement of the BAF complex in the production of oligodendrocytes in the forebrain."],["dc.description.abstract","Oligodendrocytes are responsible for axon myelination in the brain and spinal cord. Generation of oligodendrocytes entails highly regulated multistage neurodevelopmental events, including proliferation, differentiation and maturation. The chromatin remodeling BAF (mSWI/SNF) complex is a notable regulator of neural development. In our previous studies, we determined the indispensability of the BAF complex scaffolding subunits BAF155 and BAF170 for neurogenesis, whereas their role in gliogenesis is unknown. Here, we show that the expression of BAF155 and BAF170 is essential for the genesis of oligodendrocytes during brain development. We report that the ablation of BAF155 and BAF170 in the dorsal telencephalic (dTel) neural progenitors or in oligodendrocyte-producing progenitors in the ventral telencephalon (vTel) in double-conditional knockout (dcKO) mouse mutants, perturbed the process of oligodendrogenesis. Molecular marker and cell cycle analyses revealed impairment of oligodendrocyte precursor specification and proliferation, as well as overt depletion of oligodendrocytes pool in dcKO mutants. Our findings unveil a central role of BAF155 and BAF170 in oligodendrogenesis, and thus substantiate the involvement of the BAF complex in the production of oligodendrocytes in the forebrain."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3389/fcell.2021.619538"],["dc.identifier.pmid","34336815"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88908"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/409"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/151"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-455"],["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","2296-634X"],["dc.relation.orgunit","Institut für Neuroanatomie"],["dc.relation.workinggroup","RG A. Fischer (Epigenetics and Systems Medicine in Neurodegenerative Diseases)"],["dc.rights","CC BY 4.0"],["dc.title","Conditional Loss of BAF (mSWI/SNF) Scaffolding Subunits Affects Specification and Proliferation of Oligodendrocyte Precursors in Developing Mouse Forebrain"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","39"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Frontiers in Molecular Neuroscience"],["dc.bibliographiccitation.lastpage","13"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Rao, Pooja"],["dc.contributor.author","Benito-Garagorri, Eva"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:48:20Z"],["dc.date.available","2017-09-07T11:48:20Z"],["dc.date.issued","2013"],["dc.description.abstract","For many neurological diseases, the efficacy and outcome of treatment depend on early detection. Diagnosis is currently based on the detection of symptoms and neuroimaging abnormalities, which appear at relatively late stages in the pathogenesis. However, the underlying molecular responses to genetic and environmental insults begin much earlier and non-coding RNA networks are critically involved in these cellular regulatory mechanisms. Profiling RNA expression patterns could thus facilitate presymptomatic disease detection. Obtaining indirect readouts of pathological processes is particularly important for brain disorders because of the lack of direct access to tissue for molecular analyses. Living neurons and other CNS cells secrete microRNA and other small non-coding RNA into the extracellular space packaged in exosomes, microvesicles, or lipoprotein complexes. This discovery, together with the rapidly evolving massive sequencing technologies that allow detection of virtually all RNA species from small amounts of biological material, has allowed significant progress in the use of extracellular RNA as a biomarker for CNS malignancies, neurological, and psychiatric diseases. There is also recent evidence that the interactions between external stimuli and brain pathological processes may be reflected in peripheral tissues, facilitating their use as potential diagnostic markers. In this review, we explore the possibilities and challenges of using microRNA and other small RNAs as a signature for neurodegenerative and other neuropsychatric conditions."],["dc.identifier.doi","10.3389/fnmol.2013.00039"],["dc.identifier.gro","3142423"],["dc.identifier.isi","000209202800038"],["dc.identifier.pmid","24324397"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10685"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8119"],["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","1662-5099"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","MicroRNAs as biomarkers for CNS disease"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","322"],["dc.bibliographiccitation.journal","Frontiers in Cellular and Infection Microbiology"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Heimesaat, Markus M."],["dc.contributor.author","Grundmann, Ursula"],["dc.contributor.author","Alutis, Marie E."],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Bereswill, Stefan"],["dc.date.accessioned","2018-04-23T11:47:16Z"],["dc.date.available","2018-04-23T11:47:16Z"],["dc.date.issued","2017"],["dc.description.abstract","Human Campylobacter jejuni-infections are progressively increasing worldwide. Despite their high prevalence and socioeconomic impact the underlying mechanisms of pathogen-host-interactions are only incompletely understood. Given that the innate immune receptor nucleotide-oligomerization-domain-2 (Nod2) is involved in clearance of enteropathogens, we here evaluated its role in murine campylobacteriosis. To address this, we applied Nod2-deficient IL-10−/− (Nod2−/− IL-10−/−) mice and IL-10−/− counterparts both with a depleted intestinal microbiota to warrant pathogen-induced enterocolitis. At day 7 following peroral C. jejuni strain 81–176 infection, Nod2 mRNA was down-regulated in the colon of secondary abiotic IL-10−/− and wildtype mice. Nod2-deficiency did neither affect gastrointestinal colonization nor extra-intestinal and systemic translocation properties of C. jejuni. Colonic mucin-2 mRNA was, however, down-regulated upon C. jejuni-infection of both Nod2−/− IL-10−/− and IL-10−/− mice, whereas expression levels were lower in infected, but also naive Nod2−/− IL-10−/− mice as compared to respective IL-10−/− controls. Remarkably, C. jejuni-infected Nod2−/− IL-10−/− mice were less compromised than IL-10−/− counterparts and displayed less distinct apoptotic, but higher regenerative cell responses in colonic epithelia. Conversely, innate as well as adaptive immune cells such as macrophages and monocytes as well as T lymphocytes and regulatory T-cells, respectively, were even more abundant in large intestines of Nod2−/− IL-10−/− as compared to IL-10−/− mice at day 7 post-infection. Furthermore, IFN-γ concentrations were higher in ex vivo biopsies derived from intestinal compartments including colon and mesenteric lymph nodes as well as in systemic tissue sites such as the spleen of C. jejuni infected Nod2−/− IL-10−/− as compared to IL10−/− counterparts. Whereas, at day 7 postinfection anti-inflammatory IL-22 mRNA levels were up-regulated, IL-18 mRNA was down-regulated in large intestines of Nod2−/− IL-10−/− vs. IL-10−/− mice. In summary, C. jejuni-infection induced less clinical signs and apoptosis, but more distinct colonic pro- and (of note) anti-inflammatory immune as well as regenerative cell responses in Nod2 deficient IL-10−/− as compared to IL-10−/− control mice. We conclude that, even though colonic Nod2 mRNA was down-regulated upon pathogenic challenge, Nod2-signaling is essentially involved in the well-balanced innate and adaptive immune responses upon C. jejuni-infection of secondary abiotic IL-10−/− mice, but does neither impact pathogenic colonization nor translocation."],["dc.identifier.doi","10.3389/fcimb.2017.00322"],["dc.identifier.gro","3142197"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13317"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","2235-2988"],["dc.title","Absence of Nucleotide-Oligomerization-Domain-2 Is Associated with Less Distinct Disease in Campylobacter jejuni Infected Secondary Abiotic IL-10 Deficient Mice"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","33"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Gut Pathogens"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Bereswill, Stefan"],["dc.contributor.author","Grundmann, Ursula"],["dc.contributor.author","Alutis, Marie E."],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Kühl, Anja A."],["dc.contributor.author","Heimesaat, Markus M."],["dc.date.accessioned","2018-04-23T11:47:17Z"],["dc.date.available","2018-04-23T11:47:17Z"],["dc.date.issued","2017"],["dc.description.abstract","Background Campylobacter jejuni infections are of rising importance worldwide. Given that innate immune receptors including nucleotide-oligomerization-domain-2 (Nod2) are essentially involved in combating enteropathogenic infections, we here surveyed the impact of Nod2 in murine campylobacteriosis. Methods and results In order to overcome physiological colonization resistance preventing from C. jejuni infection, we generated secondary abiotic Nod2−/− and wildtype (WT) mice by broad-spectrum antibiotic treatment. Mice were then perorally infected with C. jejuni strain 81-176 on 2 consecutive days and could be stably colonized by the pathogen at high loads. Notably, Nod2 deficiency did not affect gastrointestinal colonization properties of C. jejuni. Despite high intestinal pathogenic burdens mice were virtually uncompromised and exhibited fecal blood in single cases only. At day 7 postinfection (p.i.) similar increases in numbers of colonic epithelial apoptotic cells could be observed in mice of either genotype, whereas C. jejuni infected Nod2−/− mice displayed more distinct regenerative properties in the colon than WT controls. C. jejuni infection was accompanied by increases in distinct immune cell populations such as T lymphocytes and regulatory T cells in mice of either genotype. Increases in T lymphocytes, however, were less pronounced in large intestines of Nod2−/− mice at day 7 p.i. when compared to WT mice, whereas colonic numbers of B lymphocytes were elevated in WT controls only upon C. jejuni infection. At day 7 p.i., colonic pro-inflammatory mediators including nitric oxide, TNF, IFN-γ and IL-22 increased more distinctly in Nod2−/− as compared to WT mice, whereas C. jejuni induced IL-23p19 and IL-18 levels were lower in the large intestines of the former. Converse to the colon, however, ileal concentrations of nitric oxide, TNF, IFN-γ, IL-6 and IL-10 were lower in Nod2−/− as compared to WT mice at day 7 p.i. Even though MUC2 was down-regulated in C. jejuni infected Nod2−/− mice, this did not result in increased pathogenic translocation from the intestinal tract to extra-intestinal compartments. Conclusion In secondary abiotic mice, Nod2 signaling is involved in the orchestrated host immune responses upon C. jejuni infection, but does not control pathogen loads in the gastrointestinal tract."],["dc.identifier.doi","10.1186/s13099-017-0182-0"],["dc.identifier.gro","3142199"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13319"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","1757-4749"],["dc.title","Immune responses upon Campylobacter jejuni infection of secondary abiotic mice lacking nucleotide-oligomerization-domain-2"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","825"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","838"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Pang, Petti"],["dc.contributor.author","Lu, Bai"],["dc.contributor.author","Tsai, Li-Huei"],["dc.date.accessioned","2017-09-07T11:53:39Z"],["dc.date.available","2017-09-07T11:53:39Z"],["dc.date.issued","2005"],["dc.description.abstract","While deregulation of cyclin-dependent kinase 5 (Cdk5) has been implicated in neurodegenerative diseases, its precise role in synaptic plasticity and memory remains elusive. Proteolytic cleavage of p35, a regulatory subunit of Cdk5, by calpain results in the generation of the truncated p25 protein, which causes hyperactivation of Cdk5. Using region-specific and inducible transgenic mice, we show that transiently increased p25 expression in the hippocampus enhanced long-term potentiation (LTP) and facilitated hippocampus-dependent memory. Moreover, p25 expression increased the number of dendritic spines and synapses. Importantly, enhanced memory achieved by a transient expression of p25 followed by its repression did not cause neurodegeneration. In contrast, prolonged p25 production caused severe cognitive deficits, which were accompanied by synaptic and neuronal loss and impaired LTP. Our data suggest a role for p25 in synaptic plasticity, synaptogenesis, learning, and memory and provide a model whereby deregulation of a plasticity factor can contribute to neurodegeneration."],["dc.identifier.doi","10.1016/j.neuron.2005.10.033"],["dc.identifier.gro","3143777"],["dc.identifier.isi","000233927300020"],["dc.identifier.pmid","16337919"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1328"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Intramural NIH HHS; NINDS NIH HHS [NS051874]"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0896-6273"],["dc.title","Opposing roles of transient and prolonged expression of p25 in synaptic plasticity and hippocampus-dependent memory"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","103"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Genome Biology"],["dc.bibliographiccitation.lastpage","3"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Stilling, Roman Manuel"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2017-09-07T11:45:03Z"],["dc.date.available","2017-09-07T11:45:03Z"],["dc.date.issued","2011"],["dc.description.abstract","A genetic study in Drosophila gives important insights into the epigenetic control of gene expression implicated in a human mental retardation syndrome."],["dc.identifier.doi","10.1186/gb-2011-12-2-103"],["dc.identifier.gro","3142798"],["dc.identifier.isi","000289365600001"],["dc.identifier.pmid","21320297"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8167"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/242"],["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","1474-7596"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","A Drosophila model for the role of epigenetics in brain function and development"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","letter_note"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]