Walter, Arne

[["dc.bibliographiccitation.journal","Glia"],["dc.contributor.author","Fassbender, Klaus"],["dc.contributor.author","Walter, S."],["dc.contributor.author","Kuhl, S."],["dc.contributor.author","Liu, Y."],["dc.contributor.author","Muehlhauser, F."],["dc.contributor.author","Landmann, R."],["dc.contributor.author","Ulmer, T. K."],["dc.contributor.author","Beyreuther, K."],["dc.date.accessioned","2018-11-07T10:36:31Z"],["dc.date.available","2018-11-07T10:36:31Z"],["dc.date.issued","2003"],["dc.format.extent","16"],["dc.identifier.isi","000184938300065"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45345"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.publisher.place","New york"],["dc.relation.conference","6th European Meeting on Glial Cell Function in Health and Disease"],["dc.relation.eventlocation","BERLIN, GERMANY"],["dc.relation.issn","0894-1491"],["dc.title","Mechanisms of microglial activation by Alzheimer amyloid peptide"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Stroke"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Fassbender, Klaus"],["dc.contributor.author","Walter, S."],["dc.contributor.author","Liu, Y."],["dc.contributor.author","Muehlhauser, F."],["dc.contributor.author","Ragoschke, A."],["dc.contributor.author","Kuehl, Sarah"],["dc.contributor.author","Mielke, O."],["dc.date.accessioned","2018-11-07T10:38:49Z"],["dc.date.available","2018-11-07T10:38:49Z"],["dc.date.issued","2003"],["dc.format.extent","E44"],["dc.identifier.doi","10.1161/01.STR.0000075573.22885.3B"],["dc.identifier.isi","000183348300057"],["dc.identifier.pmid","12750527"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45898"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0039-2499"],["dc.title","\"Mobile stroke unit\" for hyperacute stroke treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","167"],["dc.bibliographiccitation.issue","3-4"],["dc.bibliographiccitation.journal","Cellular Physiology and Biochemistry"],["dc.bibliographiccitation.lastpage","172"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Walter, S."],["dc.contributor.author","Doering, A."],["dc.contributor.author","Letiembre, Maryse"],["dc.contributor.author","Liu, Y."],["dc.contributor.author","Hao, W. L."],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Bernreuther, Christian"],["dc.contributor.author","Glatzel, Markus"],["dc.contributor.author","Engelhardt, B."],["dc.contributor.author","Fassbender, Klaus"],["dc.date.accessioned","2018-11-07T10:31:53Z"],["dc.date.available","2018-11-07T10:31:53Z"],["dc.date.issued","2006"],["dc.description.abstract","Innate immune receptors are crucial for defense against microorganisms. Recently, a cross-talk between innate and adaptive immunity has been considered. Here, we provide first evidence for a role of the key innate immune receptor, LPS receptor (CD14) in pathophysiology of experimental autoimmune encephalomyelitis, the animal model of multiple sclerosis. Indicating a functional importance in vivo, we show that CD14 deficiency increased clinical symptoms in active experimental autoimmune encephalomyelitis. Consistent with these observations, CD14 deficient mice exhibited a markedly enhanced infiltration of monocytes and neutrophils in brain and spinal cord. Moreover, we observed an increased immunoreactivity of CD14 in biopsy and post mortem brain tissues of multiple sclerosis patients compared to age-matched controls. Thus, the key innate immune receptor, CD14, may be of pathophysiological relevance in experimental autoimmune encephalomyelitis and multiple sclerosis."],["dc.identifier.doi","10.1159/000092078"],["dc.identifier.isi","000236127700008"],["dc.identifier.pmid","16543733"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44213"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1421-9778"],["dc.relation.issn","1015-8987"],["dc.title","The LPS receptor, CD14 in experimental autoimmune encephalomyelitis and multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1778"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","1789"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Liu, Y."],["dc.contributor.author","Walter, S."],["dc.contributor.author","Stagi, Massimiliano"],["dc.contributor.author","Cherny, D."],["dc.contributor.author","Letiembre, Maryse"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Heine, H."],["dc.contributor.author","Penke, B."],["dc.contributor.author","Neumann, H."],["dc.contributor.author","Fassbender, Klaus"],["dc.date.accessioned","2018-11-07T10:56:58Z"],["dc.date.available","2018-11-07T10:56:58Z"],["dc.date.issued","2005"],["dc.description.abstract","The amyloid beta peptide 42 (A beta(42)) plays a key role in neurotoxicity in Alzheimer's disease. Mononuclear phagocytes, i.e. microglia, have the potential to clear A beta by phagocytosis. Recently, the lipopolysaccharide (LPS) receptor CD14 was shown to mediate phagocytosis of bacterial components and furthermore to contribute to neuroinflammation in Alzheimer's disease. Here, we investigated whether this key innate immunity receptor can interact with A beta(42) and mediate phagocytosis of this peptide. Using flow cytometry, confocal microscopy and two-photon fluorescence lifetime imaging (FLIM) combined with fluorescence resonance energy transfer (FRET), we demonstrated a direct molecular interaction in the range of a few nanometers between A beta(42) and CD14 in human CD14-transfected Chinese hamster ovary cells. Investigations using cells that were genetically deficient for this receptor showed that in < 30 minutes exogenous A beta(42) added to cultured primary microglial cells was phagocytosed into the cytoplasmic compartment in a CD14-dependent manner. This phagocytosis occurred at A beta(42) concentration ranges that were considerably lower than the threshold to activate a cellular inflammatory reaction. In contrast, there was no association of CD14 to microglial internalization of microbeads. In complementary clinical experiments, we detected a pronounced CD14 immunoreactivity on parenchymal microglia spatially correlated to characteristic Alzheimer's disease lesion sites in brain sections of Alzheimer's disease patients but not in brain sections of control subjects. By showing a close interaction between CD14 and A beta(42), demonstrating a direct role of CD14 in A beta(42) phagocytosis, and detecting CD14-specific staining in brains of Alzheimer's disease patients, our results indicate a role of the LPS receptor in the pathophysiology of Alzheimer's disease, which could be of therapeutic relevance."],["dc.identifier.doi","10.1093/brain/awh531"],["dc.identifier.isi","000230724500005"],["dc.identifier.pmid","15857927"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50137"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1460-2156"],["dc.relation.issn","0006-8950"],["dc.title","LPS receptor (CD14): a receptor for phagocytosis of Alzheimer's amyloid peptide"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","203"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The FASEB Journal"],["dc.bibliographiccitation.lastpage","205"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Fassbender, Klaus"],["dc.contributor.author","Walter, S."],["dc.contributor.author","Kuhl, S."],["dc.contributor.author","Landmann, R."],["dc.contributor.author","Ishii, Kenji"],["dc.contributor.author","Bertsch, Thomas"],["dc.contributor.author","Stalder, A. K."],["dc.contributor.author","Muehlhauser, F."],["dc.contributor.author","Liu, Y."],["dc.contributor.author","Ulmer, A. J."],["dc.contributor.author","Rivest, S."],["dc.contributor.author","Lentschat, A."],["dc.contributor.author","Gulbins, E."],["dc.contributor.author","Jucker, M."],["dc.contributor.author","Staufenbiel, M."],["dc.contributor.author","Brechtel, K."],["dc.contributor.author","Walter, J."],["dc.contributor.author","Multhaup, G."],["dc.contributor.author","Penke, B."],["dc.contributor.author","Adachi, Y."],["dc.contributor.author","Hartmann, T."],["dc.contributor.author","Beyreuther, K."],["dc.date.accessioned","2018-11-07T10:52:30Z"],["dc.date.available","2018-11-07T10:52:30Z"],["dc.date.issued","2004"],["dc.description.abstract","To rapidly respond to invading microorganisms, humans call on their innate immune system. This occurs by microbe-detecting receptors, such as CD14, that activate immune cells to eliminate the pathogens. Here, we link the lipopolysaccharide receptor CD14 with Alzheimer's disease, a severe neurodegenerative disease resulting in dementia. We demonstrate that this key innate immunity receptor interacts with fibrils of Alzheimer amyloid peptide. Neutralization with antibodies against CD14 and genetic deficiency for this receptor significantly reduced amyloid peptide induced microglial activation and microglial toxicity. The observation of strongly enhanced microglial expression of the LPS receptor in brains of animal models of Alzheimer's disease indicates a clinical relevance of these findings. These data suggest that CD14 may significantly contribute to the overall neuroinflammatory response to amyloid peptide, highlighting the possibility that the enormous progress currently being made in the field of innate immunity could be extended to research on Alzheimer's disease."],["dc.identifier.doi","10.1096/fj.03-0364fje"],["dc.identifier.isi","000188829300074"],["dc.identifier.pmid","14597556"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49128"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Federation Amer Soc Exp Biol"],["dc.relation.issn","1530-6860"],["dc.relation.issn","0892-6638"],["dc.title","The LPS receptor (CD14) links innate immunity with Alzheimer's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","248"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuroscience"],["dc.bibliographiccitation.lastpage","254"],["dc.bibliographiccitation.volume","146"],["dc.contributor.author","Letiembre, Maryse"],["dc.contributor.author","Hao, Wenlin"],["dc.contributor.author","Liu, Y."],["dc.contributor.author","Walter, S."],["dc.contributor.author","Mihaljevic, I."],["dc.contributor.author","Rivest, S."],["dc.contributor.author","Hartmann, T."],["dc.contributor.author","Fassbender, Klaus"],["dc.date.accessioned","2018-11-07T11:03:09Z"],["dc.date.available","2018-11-07T11:03:09Z"],["dc.date.issued","2007"],["dc.description.abstract","Brain aging often results in cognitive impairment and is considered to be a major risk factor for neurodegenerative diseases. Earlier studies reported inflammatory responses in aged brain that could contribute to age-related neurodegeneration. Recently, innate immune receptors such as toll-like receptors (TLRs), so far implicated in defense against microorganisms, have been linked to pathogenesis of Alzheimer's disease. Therefore, we asked whether the transcription of TLRs (1-9) and CD14, could also be altered in physiological brain aging. Using real-time polymerase chain reaction (PCR), we indeed observed that TLR1, TLR2, TLR4, TLR5, TLR7 and CD14 expression was up-regulated in mouse brain in correlation with age. In contrast, transcriptions of TLR3, TLR6 and TLR8 were unchanged and the one of TLR9 was down-regulated. In situ hybridization further confirmed these results and identified the cellular source of TLR2 and TLR7 as mononuclear phagocytes. Together, this first systematic analysis demonstrates altered regulation of those innate immune receptors even in normal brain aging, which might be of relevance for understanding susceptibility to neurodegenerative processes associated with aging. (c) 2007 IBRO. Published by Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neuroscience.2007.01.004"],["dc.identifier.isi","000246410700025"],["dc.identifier.pmid","17293054"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51552"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","1873-7544"],["dc.relation.issn","0306-4522"],["dc.title","Innate immune receptor expression in normal brain aging"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]