Walter, Arne

[["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","154"],["dc.contributor.author","Walter, S."],["dc.date.accessioned","2018-11-07T10:46:03Z"],["dc.date.available","2018-11-07T10:46:03Z"],["dc.date.issued","2004"],["dc.format.extent","170"],["dc.identifier.isi","000224003200571"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47656"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","7th International Congress of the International-Society-of-Neuroimmunology"],["dc.relation.eventlocation","Venice, ITALY"],["dc.relation.issn","0165-5728"],["dc.title","Innate immunity receptor TLR4 plays a key role in Alzheimer's disease"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Glia"],["dc.contributor.author","Walter, S."],["dc.contributor.author","Heine, H."],["dc.contributor.author","Walter, J."],["dc.contributor.author","Brechtel, K."],["dc.contributor.author","Muhlhauser, F."],["dc.contributor.author","Fassbender, Klaus"],["dc.date.accessioned","2018-11-07T10:36:32Z"],["dc.date.available","2018-11-07T10:36:32Z"],["dc.date.issued","2003"],["dc.format.extent","74"],["dc.identifier.isi","000184938300324"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45350"],["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","Alzheimer beta-amyloid mediates microglial activation via Toll-like-receptor 4"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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.firstpage","14971"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Journal of Virology"],["dc.bibliographiccitation.lastpage","14975"],["dc.bibliographiccitation.volume","79"],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Buchholz, M."],["dc.contributor.author","Neubauer, A."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Groschup, M."],["dc.contributor.author","Walter, S."],["dc.contributor.author","Arendt, S."],["dc.contributor.author","Neumann, M."],["dc.contributor.author","Voss, A. K."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.date.accessioned","2018-11-07T10:53:58Z"],["dc.date.available","2018-11-07T10:53:58Z"],["dc.date.issued","2005"],["dc.description.abstract","Transmissible mink encephalopathy (TME) is a rare disease of the North American mink, which has never been successfully transmitted to laboratory mice. We generated transgenic mice expressing the mink prion protein (PrP) and inoculated them with TME or the mouse-adapted scrapie strain 79A. TME infected mink PrP-transgenic mice on a murine PrP knockout background. The absolute species barrier between the infectious agent of TME and mice was therefore broken. Following TME and 79A infection of mice carrying both mink and murine PrPC, only proteinase-resistant PrP homologous to the incoming agent was detectable. The presence of the murine PrPC prolonged the incubation time of TME substantially."],["dc.identifier.doi","10.1128/JVI.79.23.14971-14975.2005"],["dc.identifier.isi","000233279300052"],["dc.identifier.pmid","16282497"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49462"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0022-538X"],["dc.title","Breaking an absolute species barrier: Transgenic mice expressing the mink PrP gene are susceptible to transmissible mink encephalopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5136"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","The Journal of Physical Chemistry B"],["dc.bibliographiccitation.lastpage","5144"],["dc.bibliographiccitation.volume","119"],["dc.contributor.author","Walter, Arne"],["dc.contributor.author","Andresen, Martin"],["dc.contributor.author","Jakobs, Stefan"],["dc.contributor.author","Schroeder, Jörg"],["dc.contributor.author","Schwarzer, Dirk"],["dc.date.accessioned","2017-09-07T11:44:26Z"],["dc.date.available","2017-09-07T11:44:26Z"],["dc.date.issued","2015"],["dc.description.abstract","The reversible photoswitching of the photochromic fluorescent protein Padron0.9 involves a cis-trans isomerization of the chromophore. Both isomers are subjected to a protonation equilibrium between a neutral and a deprotonated form. The observed pH dependent absorption spectra require at least two protonating groups in the chromophore environment, modulating its proton affinity. Using femtosecond transient absorption spectroscopy, we elucidate the primary reaction steps of selectively excited chromophore Speties. Employing kinetic and spectral modeling of the dine dependent transients, we identify intermediate states and their spectra. Excitation of the deprotonated trans species is followed by excited state relaxation and internal conversion to a hot ground, state on a time scale of 1.1-6.5 ps. As the switching yield is very low (Phi(trans -> cis) = 0.0003 +/- 0.0001), direct formation of the cis isomer in the time-resolved experiment is not observed. The reverse switching route involves excitation of the neutral cis chromophore.. A strong H/D isotope effect reveals the initial reaction step to be an excited State proton transfer with a rate constant of k(H) = (1.7 ps)(-1) (k(D) = (8.6 ps)(-1)) competing with internal conversion (k(ic) = (4.5 ps)(-1)). The deprotonated excited cis intermediate relaxes to the well-known long-lived fluorescent species (k(r) = (24 ps)(-1)). The switching quantum yield is determined to be low as well, Phi(cis -> trans) = 0.02 +/- 0.01. Excitation of both the neutral and deprotonated cis chromophores is followed by a ground state proton transfer reaction partially re-establishing the disturbed ground state equilibrium within 1.6 ps (deuterated species: 5.6 ps). The incomplete equilibration reveals an inhomogeneous population of deprotonated cis species which equilibrate on different time scales."],["dc.identifier.doi","10.1021/jp512610q"],["dc.identifier.gro","3141920"],["dc.identifier.isi","000353604800004"],["dc.identifier.pmid","25802098"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2544"],["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","1520-6106"],["dc.title","Primary Light-Induced Reaction Steps of Reversibly Photoswitchable Fluorescent Protein Padron0.9 Investigated by Femtosecond Spectroscopy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["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.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","154"],["dc.contributor.author","Wagner, S."],["dc.contributor.author","Mossner, Rotraut"],["dc.contributor.author","Walter, S."],["dc.contributor.author","Fassbender, Klaus"],["dc.date.accessioned","2018-11-07T10:46:02Z"],["dc.date.available","2018-11-07T10:46:02Z"],["dc.date.issued","2004"],["dc.format.extent","117"],["dc.identifier.isi","000224003200397"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47652"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","7th International Congress of the International-Society-of-Neuroimmunology"],["dc.relation.eventlocation","Venice, ITALY"],["dc.relation.issn","0165-5728"],["dc.title","Influence of PPAR-gamma agonists on prion-protein induced microglia activation"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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"]]