Walter, Arne

[["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.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","1257"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","1258"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Fassbender, K."],["dc.contributor.author","Stroick, M."],["dc.contributor.author","Bertsch, T."],["dc.contributor.author","Ragoschke, A."],["dc.contributor.author","Kuehl, S."],["dc.contributor.author","Walter, S."],["dc.contributor.author","Walter, J."],["dc.contributor.author","Brechtel, K."],["dc.contributor.author","Muehlhauser, F."],["dc.contributor.author","Lutjohann, D."],["dc.date.accessioned","2021-06-01T10:48:13Z"],["dc.date.available","2021-06-01T10:48:13Z"],["dc.date.issued","2002"],["dc.description.abstract","Cerebral cholesterol metabolism has been linked with production of amyloid peptide (Abeta) crucial in AD. The association between use of cholesterol-lowering drugs (statins) and AD disease is currently being intensely discussed. In this case-control study on elderly nondemented subjects, the authors provide the first evidence that statins in clinically relevant dosages indeed affect cerebral cholesterol metabolism. However, these changes were not associated with altered intrathecal secretion of Alzheimer Abeta."],["dc.identifier.doi","10.1212/WNL.59.8.1257"],["dc.identifier.isi","000178726700027"],["dc.identifier.pmid","12391360"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85859"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.eissn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Effects of statins on human cerebral cholesterol metabolism and secretion of Alzheimer amyloid peptide"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]