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Griesinger, Christian
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Griesinger, Christian
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Griesinger, Christian
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Griesinger, C.
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2014Journal Article Discussion [["dc.bibliographiccitation.firstpage","779"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","780"],["dc.bibliographiccitation.volume","127"],["dc.contributor.author","Levin, Johannes"],["dc.contributor.author","Schmidt, Felix"],["dc.contributor.author","Boehm, Cathrin"],["dc.contributor.author","Prix, Catharina"],["dc.contributor.author","Boetzel, Kai"],["dc.contributor.author","Ryazanov, Sergey"],["dc.contributor.author","Leonov, Andrei"],["dc.contributor.author","Griesinger, Christian"],["dc.contributor.author","Giese, Armin"],["dc.date.accessioned","2017-09-07T11:46:17Z"],["dc.date.available","2017-09-07T11:46:17Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1007/s00401-014-1265-3"],["dc.identifier.gro","3142137"],["dc.identifier.isi","000334426300011"],["dc.identifier.pmid","24615514"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12109"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/4955"],["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.publisher","Springer"],["dc.relation.eissn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","The oligomer modulator anle138b inhibits disease progression in a Parkinson mouse model even with treatment started after disease onset"],["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"]]Details DOI PMID PMC WOS2019Journal Article Research Paper [["dc.bibliographiccitation.firstpage","575"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","595"],["dc.bibliographiccitation.volume","138"],["dc.contributor.author","Wegrzynowicz, Michal"],["dc.contributor.author","Bar-On, Dana"],["dc.contributor.author","Calo’, Laura"],["dc.contributor.author","Anichtchik, Oleg"],["dc.contributor.author","Iovino, Mariangela"],["dc.contributor.author","Xia, Jing"],["dc.contributor.author","Ryazanov, Sergey"],["dc.contributor.author","Leonov, Andrei"],["dc.contributor.author","Giese, Armin"],["dc.contributor.author","Dalley, Jeffrey W."],["dc.contributor.author","Griesinger, Christian"],["dc.contributor.author","Ashery, Uri"],["dc.contributor.author","Spillantini, Maria Grazia"],["dc.date.accessioned","2020-12-10T14:10:27Z"],["dc.date.available","2020-12-10T14:10:27Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s00401-019-02023-x"],["dc.identifier.pmid","31165254"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16591"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70765"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/28"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.workinggroup","RG Griesinger"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Depopulation of dense α-synuclein aggregates is associated with rescue of dopamine neuron dysfunction and death in a new Parkinson’s disease model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2019Journal Article Research Paper [["dc.bibliographiccitation.firstpage","255"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Movement Disorders"],["dc.bibliographiccitation.lastpage","263"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Heras-Garvin, Antonio"],["dc.contributor.author","Weckbecker, Daniel"],["dc.contributor.author","Ryazanov, Sergey"],["dc.contributor.author","Leonov, Andrei"],["dc.contributor.author","Griesinger, Christian"],["dc.contributor.author","Giese, Armin"],["dc.contributor.author","Wenning, Gregor K."],["dc.contributor.author","Stefanova, Nadia"],["dc.date.accessioned","2022-02-21T11:05:20Z"],["dc.date.available","2022-02-21T11:05:20Z"],["dc.date.issued","2019"],["dc.description.abstract","MSA is a fatal neurodegenerative disease characterized by autonomic failure and severe motor impairment. Its main pathological hallmark is the accumulation of α-synuclein in oligodendrocytes, leading to glial and neuronal dysfunction and neurodegeneration. These features are recapitulated in the PLP-hαSyn mouse model expressing human α-synuclein in oligodendrocytes. At present, there is no effective disease-modifying therapy. Previous experiments have shown that the aggregation inhibitor, anle138b, reduces neurodegeneration and behavioral deficits in mouse models of other proteinopathies."],["dc.identifier.doi","10.1002/mds.27562"],["dc.identifier.pmid","30452793"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/100131"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/210"],["dc.language.iso","en"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.eissn","1531-8257"],["dc.relation.issn","0885-3185"],["dc.relation.workinggroup","RG Griesinger"],["dc.rights","CC BY 4.0"],["dc.title","Anle138b modulates α-synuclein oligomerization and prevents motor decline and neurodegeneration in a mouse model of multiple system atrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2020Journal Article Research Paper [["dc.bibliographiccitation.journal","European Journal of Nuclear Medicine and Molecular Imaging"],["dc.contributor.author","Kuebler, Laura"],["dc.contributor.author","Buss, Sabrina"],["dc.contributor.author","Leonov, Andrei"],["dc.contributor.author","Ryazanov, Sergey"],["dc.contributor.author","Schmidt, Felix"],["dc.contributor.author","Maurer, Andreas"],["dc.contributor.author","Weckbecker, Daniel"],["dc.contributor.author","Landau, Anne M."],["dc.contributor.author","Lillethorup, Thea P."],["dc.contributor.author","Bleher, Daniel"],["dc.contributor.author","Saw, Ran Sing"],["dc.contributor.author","Pichler, Bernd J."],["dc.contributor.author","Griesinger, Christian"],["dc.contributor.author","Giese, Armin"],["dc.contributor.author","Herfert, Kristina"],["dc.date.accessioned","2021-04-14T08:30:50Z"],["dc.date.available","2021-04-14T08:30:50Z"],["dc.date.issued","2020"],["dc.description.abstract","Purpose\r\n\r\nDeposition of misfolded alpha-synuclein (αSYN) aggregates in the human brain is one of the major hallmarks of synucleinopathies. However, a target-specific tracer to detect pathological aggregates of αSYN remains lacking. Here, we report the development of a positron emission tomography (PET) tracer based on anle138b, a compound shown to have therapeutic activity in animal models of neurodegenerative diseases.\r\nMethods\r\n\r\nSpecificity and selectivity of [3H]MODAG-001 were tested in in vitro binding assays using recombinant fibrils. After carbon-11 radiolabeling, the pharmacokinetic and metabolic profile was determined in mice. Specific binding was quantified in rats, inoculated with αSYN fibrils and using in vitro autoradiography in human brain sections of Lewy body dementia (LBD) cases provided by the Neurobiobank Munich (NBM).\r\nResults\r\n\r\n[3H]MODAG-001 revealed a very high affinity towards pure αSYN fibrils (Kd = 0.6 ± 0.1 nM) and only a moderate affinity to hTau46 fibrils (Kd = 19 ± 6.4 nM) as well as amyloid-β1–42 fibrils (Kd = 20 ± 10 nM). [11C]MODAG-001 showed an excellent ability to penetrate the mouse brain. Metabolic degradation was present, but the stability of the parent compound improved after selective deuteration of the precursor. (d3)-[11C]MODAG-001 binding was confirmed in fibril-inoculated rat striata using in vivo PET imaging. In vitro autoradiography showed no detectable binding to aggregated αSYN in human brain sections of LBD cases, most likely, because of the low abundance of aggregated αSYN against background protein.\r\nConclusion\r\n\r\nMODAG-001 provides a promising lead structure for future compound development as it combines a high affinity and good selectivity in fibril-binding assays with suitable pharmacokinetics and biodistribution properties."],["dc.identifier.doi","10.1007/s00259-020-05133-x"],["dc.identifier.pmid","33369690"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83387"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/101"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.eissn","1619-7089"],["dc.relation.issn","1619-7070"],["dc.relation.workinggroup","RG Griesinger"],["dc.rights","CC BY 4.0"],["dc.title","[11C]MODAG-001—towards a PET tracer targeting α-synuclein aggregates"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2019Journal Article [["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Bartels, Martin"],["dc.contributor.author","Weckbecker, Daniel"],["dc.contributor.author","Kuhn, Peer-Hendrik"],["dc.contributor.author","Ryazanov, Sergey"],["dc.contributor.author","Leonov, Andrei"],["dc.contributor.author","Griesinger, Christian"],["dc.contributor.author","Lichtenthaler, Stefan F."],["dc.contributor.author","Bötzel, Kai"],["dc.contributor.author","Giese, Armin"],["dc.date.accessioned","2020-12-10T18:10:13Z"],["dc.date.available","2020-12-10T18:10:13Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1038/s41598-019-45298-6"],["dc.identifier.eissn","2045-2322"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16341"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73892"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Iron-mediated aggregation and toxicity in a novel neuronal cell culture model with inducible alpha-synuclein expression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI2016Journal Article Research Paper [["dc.bibliographiccitation.artnumber","99"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Frontiers in Neuroscience"],["dc.bibliographiccitation.lastpage","9"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Fellner, Lisa"],["dc.contributor.author","Kuzdas-Wood, Daniela"],["dc.contributor.author","Levin, Johannes"],["dc.contributor.author","Ryazanov, Sergey"],["dc.contributor.author","Leonov, Andrei"],["dc.contributor.author","Griesinger, Christian"],["dc.contributor.author","Giese, Armin"],["dc.contributor.author","Wenning, Gregor K."],["dc.contributor.author","Stefanova, Nadia"],["dc.date.accessioned","2017-09-07T11:54:34Z"],["dc.date.available","2017-09-07T11:54:34Z"],["dc.date.issued","2016"],["dc.description.abstract","The neurodegenerative disorder multiple system atrophy (MSA) is characterized by autonomic failure, cerebellar ataxia and parkinsonism in any combination associated with predominantly oligodendroglial alpha-synuclein (alpha-syn) aggregates (glial cytoplasmic inclusions = GCls). To date, there is no effective disease modifying therapy. Previous experiments have shown that the aggregation inhibitor anle138b reduces neurodegeneration, as well as behavioral deficits in both transgenic and toxin mouse models of Parkinson's disease (PD). Here we analyzed whether anle138b improves motor skills and reduces neuronal loss, as well as oligodendroglial alpha-syn aggregation in the PLP-alpha-syn transgenic mouse challenged with the mitochondria' toxin 3-nitropropionic acid (3-NP) to model full-blown MSA. Following 1 month of treatment with anle138b, MSA mice showed signs of motor improvement affecting stride length, but not pole, grip strength, and beam test performance. Loss of dopaminergic nigral neurons and Purkinje cells was not attenuated and GCI density remained unchanged. These data suggest that the pathology in transgenic PLP-alpha-syn mice receiving 3-NP might be too advanced to detect significant effects of anle138b treatment on neuronal loss and intracytoplasmic alpha-syn inclusion bodies. However, the partial motor amelioration may indicate potential efficacy of anle138b treatment that may be mediated by its actions on alpha-syn oligomers or may reflect improvement of neuronal dysfunction in neural at risk populations. Further studies are required to address the efficacy of anle138b in transgenic alpha-syn models of early-stage MSA and in the absence of additional toxin application."],["dc.identifier.doi","10.3389/fnins.2016.00099"],["dc.identifier.gro","3141710"],["dc.identifier.isi","000371761400001"],["dc.identifier.pmid","27013960"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13156"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/213"],["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","1662-453X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Anle138b Partly Ameliorates Motor Deficits Despite Failure of Neuroprotection in a Model of Advanced Multiple System Atrophy"],["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"]]Details DOI PMID PMC WOS2017-12-05Journal Article [["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"]]Details DOI PMID PMC2019Journal Article Research Paper [["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Saravanan, Manikam S."],["dc.contributor.author","Ryazanov, Sergey"],["dc.contributor.author","Leonov, Andrei"],["dc.contributor.author","Nicolai, Janine"],["dc.contributor.author","Praest, Patrique"],["dc.contributor.author","Giese, Armin"],["dc.contributor.author","Winter, Roland"],["dc.contributor.author","Khemtemourian, Lucie"],["dc.contributor.author","Griesinger, Christian"],["dc.contributor.author","Killian, J. Antoinette"],["dc.date.accessioned","2020-12-10T18:11:10Z"],["dc.date.available","2020-12-10T18:11:10Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1038/s41598-019-54919-z"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17084"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73911"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/18"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.workinggroup","RG Griesinger"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The small molecule inhibitor anle145c thermodynamically traps human islet amyloid peptide in the form of non-cytotoxic oligomers"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI2020Journal Article Research Paper [["dc.bibliographiccitation.firstpage","411"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","ChemMedChem"],["dc.bibliographiccitation.lastpage","415"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Maurer, Andreas"],["dc.contributor.author","Leonov, Andrei"],["dc.contributor.author","Ryazanov, Sergey"],["dc.contributor.author","Herfert, Kristina"],["dc.contributor.author","Kuebler, Laura"],["dc.contributor.author","Buss, Sabrina"],["dc.contributor.author","Schmidt, Felix"],["dc.contributor.author","Weckbecker, Daniel"],["dc.contributor.author","Linder, Ruth"],["dc.contributor.author","Bender, Dirk"],["dc.contributor.author","Giese, Armin"],["dc.contributor.author","Pichler, Bernd J."],["dc.contributor.author","Griesinger, Christian"],["dc.date.accessioned","2022-02-21T12:35:21Z"],["dc.date.available","2022-02-21T12:35:21Z"],["dc.date.issued","2020"],["dc.description.abstract","There is an urgent clinical need for imaging of α-synuclein (αSyn) fibrils, the hallmark biomarker for Parkinson's disease, in neurodegenerative disorders. Despite immense efforts, promising tracer candidates for nuclear imaging of αSyn are rare. Diphenyl pyrazoles are known modulators of αSyn aggregation and thus bear potential for non-invasive detection of this biomarker in vivo. Here we demonstrate high-affinity binding of the family member anle253b to fibrillar αSyn and present a high-yielding site-selective radiosynthesis route for 11 C radiolabeling using in-situ generated [11 C]formaldehyde and reductive methylation. Radio-HPLC of the tracer after incubation with rat serum in vitro shows excellent stability of the molecule. Positron emission tomography in healthy animals is used to assess the pharmacokinetics and biodistribution of the tracer, showing good penetration of the blood-brain barrier and low background binding to the non-pathological brain."],["dc.identifier.doi","10.1002/cmdc.201900689"],["dc.identifier.pmid","31859430"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/100141"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/197"],["dc.language.iso","en"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.eissn","1860-7187"],["dc.relation.issn","1860-7179"],["dc.relation.workinggroup","RG Griesinger"],["dc.rights","CC BY-NC-ND 4.0"],["dc.title","11 C Radiolabeling of anle253b: a Putative PET Tracer for Parkinson's Disease That Binds to α-Synuclein Fibrils in vitro and Crosses the Blood-Brain Barrier"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2019Journal Article Research Paper [["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Alzheimer's Research & Therapy"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Brendel, Matthias"],["dc.contributor.author","Deussing, Maximilian"],["dc.contributor.author","Blume, Tanja"],["dc.contributor.author","Kaiser, Lena"],["dc.contributor.author","Probst, Federico"],["dc.contributor.author","Overhoff, Felix"],["dc.contributor.author","Peters, Finn"],["dc.contributor.author","von Ungern-Sternberg, Barbara"],["dc.contributor.author","Ryazanov, Sergey"],["dc.contributor.author","Leonov, Andrei"],["dc.contributor.author","Griesinger, Christian"],["dc.contributor.author","Zwergal, Andreas"],["dc.contributor.author","Levin, Johannes"],["dc.contributor.author","Bartenstein, Peter"],["dc.contributor.author","Yakushev, Igor"],["dc.contributor.author","Cumming, Paul"],["dc.contributor.author","Boening, Guido"],["dc.contributor.author","Ziegler, Sibylle"],["dc.contributor.author","Herms, Jochen"],["dc.contributor.author","Giese, Armin"],["dc.contributor.author","Rominger, Axel"],["dc.date.accessioned","2020-12-10T18:39:08Z"],["dc.date.available","2020-12-10T18:39:08Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1186/s13195-019-0522-z"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16327"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77552"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/25"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.workinggroup","RG Griesinger"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Late-stage Anle138b treatment ameliorates tau pathology and metabolic decline in a mouse model of human Alzheimer’s disease tau"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI