Arnim, Christine A. F. von

[["dc.bibliographiccitation.artnumber","alz.12794"],["dc.bibliographiccitation.journal","Alzheimer's & Dementia"],["dc.contributor.author","Schaeverbeke, Jolien"],["dc.contributor.author","Tomé, Sandra O."],["dc.contributor.author","Ronisz, Alicja"],["dc.contributor.author","Ospitalieri, Simona"],["dc.contributor.author","von Arnim, Christine A. F."],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Vandenberghe, Rik"],["dc.contributor.author","Thal, Dietmar Rudolf"],["dc.date.accessioned","2022-10-04T10:21:57Z"],["dc.date.available","2022-10-04T10:21:57Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1002/alz.12794"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114547"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-600"],["dc.relation.eissn","1552-5279"],["dc.relation.issn","1552-5260"],["dc.title","Neuronal loss of the nucleus basalis of Meynert in primary progressive aphasia is associated with Alzheimer's disease neuropathological changes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","173"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","192"],["dc.bibliographiccitation.volume","141"],["dc.contributor.author","Aragão Gomes, Luis"],["dc.contributor.author","Uytterhoeven, Valerie"],["dc.contributor.author","Lopez-Sanmartin, Diego"],["dc.contributor.author","Tomé, Sandra O."],["dc.contributor.author","Tousseyn, Thomas"],["dc.contributor.author","Vandenberghe, Rik"],["dc.contributor.author","Vandenbulcke, Mathieu"],["dc.contributor.author","von Arnim, Christine A. F."],["dc.contributor.author","Verstreken, Patrik"],["dc.contributor.author","Thal, Dietmar Rudolf"],["dc.date.accessioned","2021-04-14T08:30:40Z"],["dc.date.available","2021-04-14T08:30:40Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1007/s00401-020-02251-6"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83332"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.title","Maturation of neuronal AD-tau pathology involves site-specific phosphorylation of cytoplasmic and synaptic tau preceding conformational change and fibril formation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica Communications"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Tomé, Sandra O."],["dc.contributor.author","Vandenberghe, Rik"],["dc.contributor.author","Ospitalieri, Simona"],["dc.contributor.author","Van Schoor, Evelien"],["dc.contributor.author","Tousseyn, Thomas"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","von Arnim, Christine A. F."],["dc.contributor.author","Thal, Dietmar Rudolf"],["dc.date.accessioned","2020-12-10T18:41:24Z"],["dc.date.available","2020-12-10T18:41:24Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1186/s40478-020-00934-5"],["dc.identifier.eissn","2051-5960"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17243"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77570"],["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","Distinct molecular patterns of TDP-43 pathology in Alzheimer’s disease: relationship with clinical phenotypes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica Communications"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Thal, Dietmar Rudolf"],["dc.contributor.author","Ronisz, Alicja"],["dc.contributor.author","Tousseyn, Thomas"],["dc.contributor.author","Upadhaya, Ajeet Rijal"],["dc.contributor.author","Balakrishnan, Karthikeyan"],["dc.contributor.author","Vandenberghe, Rik"],["dc.contributor.author","Vandenbulcke, Mathieu"],["dc.contributor.author","von Arnim, Christine A. F."],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Beach, Thomas G."],["dc.contributor.author","Lilja, Johan"],["dc.contributor.author","Heurling, Kerstin"],["dc.contributor.author","Chakrabarty, Aruna"],["dc.contributor.author","Ismail, Azzam"],["dc.contributor.author","Buckley, Christopher"],["dc.contributor.author","Smith, Adrian P. L."],["dc.contributor.author","Kumar, Sathish"],["dc.contributor.author","Farrar, Gill"],["dc.contributor.author","Walter, Jochen"],["dc.date.accessioned","2021-04-14T08:23:56Z"],["dc.date.available","2021-04-14T08:23:56Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1186/s40478-020-01005-5"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81101"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2051-5960"],["dc.relation.iserratumof","/handle/2/77569"],["dc.title","Correction to: Different aspects of Alzheimer’s disease-related amyloid β-peptide pathology and their relationship to amyloid positron emission tomography imaging and dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","erratum_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica Communications"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Thal, Dietmar Rudolf"],["dc.contributor.author","Ronisz, Alicja"],["dc.contributor.author","Tousseyn, Thomas"],["dc.contributor.author","Rijal Upadhaya, Ajeet"],["dc.contributor.author","Balakrishnan, Karthikeyan"],["dc.contributor.author","Vandenberghe, Rik"],["dc.contributor.author","Vandenbulcke, Mathieu"],["dc.contributor.author","von Arnim, Christine A. F."],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Beach, Thomas G."],["dc.contributor.author","Lilja, Johan"],["dc.contributor.author","Heurling, Kerstin"],["dc.contributor.author","Chakrabarty, Aruna"],["dc.contributor.author","Ismail, Azzam"],["dc.contributor.author","Buckley, Christopher"],["dc.contributor.author","Smith, Adrian P. L."],["dc.contributor.author","Kumar, Sathish"],["dc.contributor.author","Farrar, Gill"],["dc.contributor.author","Walter, Jochen"],["dc.date.accessioned","2020-12-10T18:41:24Z"],["dc.date.available","2020-12-10T18:41:24Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1186/s40478-019-0837-9"],["dc.identifier.eissn","2051-5960"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77569"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation.haserratum","/handle/2/81101"],["dc.title","Different aspects of Alzheimer’s disease-related amyloid β-peptide pathology and their relationship to amyloid positron emission tomography imaging and dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","128"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica Communications"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Koper, Marta J."],["dc.contributor.author","Tomé, Sandra O."],["dc.contributor.author","Gawor, Klara"],["dc.contributor.author","Belet, Annelies"],["dc.contributor.author","Van Schoor, Evelien"],["dc.contributor.author","Schaeverbeke, Jolien"],["dc.contributor.author","Vandenberghe, Rik"],["dc.contributor.author","Vandenbulcke, Mathieu"],["dc.contributor.author","Ghebremedhin, Estifanos"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","von Arnim, Christine A. F."],["dc.contributor.author","Balusu, Sriram"],["dc.contributor.author","Blaschko, Matthew B."],["dc.contributor.author","De Strooper, Bart"],["dc.contributor.author","Thal, Dietmar R."],["dc.date.accessioned","2022-09-05T09:03:13Z"],["dc.date.available","2022-09-05T09:03:13Z"],["dc.date.issued","2022-09-03"],["dc.date.updated","2022-09-04T03:12:22Z"],["dc.description.abstract","Abstract\r\n It has become evident that Alzheimer’s Disease (AD) is not only linked to its hallmark lesions—amyloid plaques and neurofibrillary tangles (NFTs)—but also to other co-occurring pathologies. This may lead to synergistic effects of the respective cellular and molecular players, resulting in neuronal death. One of these co-pathologies is the accumulation of phosphorylated transactive-response DNA binding protein 43 (pTDP-43) as neuronal cytoplasmic inclusions, currently considered to represent limbic-predominant age-related TDP-43 encephalopathy neuropathological changes (LATE-NC), in up to 70% of symptomatic AD cases. Granulovacuolar degeneration (GVD) is another AD co-pathology, which also contains TDP-43 and other AD-related proteins. Recently, we found that all proteins required for necroptosis execution, a previously defined programmed form of neuronal cell death, are present in GVD, such as the phosphorylated necroptosis executioner mixed-lineage kinase domain-like protein (pMLKL). Accordingly, this protein is a reliable marker for GVD lesions, similar to other known GVD proteins. Importantly, it is not yet known whether the presence of LATE-NC in symptomatic AD cases is associated with necroptosis pathway activation, presumably contributing to neuron loss by cell death execution. In this study, we investigated the impact of LATE-NC on the severity of necroptosis-associated GVD lesions, phosphorylated tau (pTau) pathology and neuronal density. First, we used 230 human post-mortem cases, including 82 controls without AD neuropathological changes (non-ADNC), 81 non-demented cases with ADNC, i.e.: pathologically-defined preclinical AD (p-preAD) and 67 demented cases with ADNC. We found that Braak NFT stage and LATE-NC stage were good predictors for GVD expansion and neuronal loss in the hippocampal CA1 region. Further, we compared the impact of TDP-43 accumulation on hippocampal expression of pMLKL-positive GVD, pTau as well as on neuronal density in a subset of nine non-ADNC controls, ten symptomatic AD cases with (ADTDP+) and eight without LATE-NC (ADTDP−). Here, we observed increased levels of pMLKL-positive, GVD-exhibiting neurons in ADTDP+ cases, compared to ADTDP− and controls, which was accompanied by augmented pTau pathology. Neuronal loss in the CA1 region was increased in ADTDP+ compared to ADTDP− cases. These data suggest that co-morbid LATE-NC in AD impacts not only pTau pathology but also GVD-mediated necroptosis pathway activation, which results in an accelerated neuronal demise. This further highlights the cumulative and synergistic effects of comorbid pathologies leading to neuronal loss in AD. Accordingly, protection against necroptotic neuronal death appears to be a promising therapeutic option for AD and LATE."],["dc.identifier.citation","Acta Neuropathologica Communications. 2022 Sep 03;10(1):128"],["dc.identifier.doi","10.1186/s40478-022-01432-6"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114073"],["dc.language.iso","en"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)"],["dc.subject","Granulovacuolar degeneration"],["dc.subject","LATE-NC"],["dc.subject","TDP-43"],["dc.subject","Necroptosis"],["dc.subject","Cell death"],["dc.subject","pMLKL"],["dc.subject","pTau"],["dc.subject","Protein aggregation"],["dc.title","LATE-NC aggravates GVD-mediated necroptosis in Alzheimer’s disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

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