Nau, Roland

[["dc.bibliographiccitation.firstpage","1877"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of Neuroscience Research"],["dc.bibliographiccitation.lastpage","1883"],["dc.bibliographiccitation.volume","87"],["dc.contributor.author","Tauber, Simone C."],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Schulz, Daniela"],["dc.contributor.author","Kellert, Benedikt"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Gerber, Joachim"],["dc.date.accessioned","2018-11-07T08:29:27Z"],["dc.date.available","2018-11-07T08:29:27Z"],["dc.date.issued","2009"],["dc.description.abstract","An increase in adult neurogenesis was observed after exposure to enriched environment (EE) and during reconvalescence from experimental pneumococcal meningitis. This study investigated neurogenesis and spatial learning performance 5 weeks after bacterial meningitis and exposure to EE. C57BL/6 mice were infected by intracerebral injection of Streptococcus pneumoniae and treated with ceftriaxone for 5 days. Forty-eight hours after infection, one group (n = 22) was exposed to EE and the other group (n = 23) housed under standard conditions. Another set of mice was kept under either enriched (n = 16) or standard (n = 15) conditions without bacterial meningitis. Five weeks later, the Morris water maze was performed, and neurogenesis was evaluated by means of immunohistochemistry. Mice housed in EE without prior bacterial infection displayed both increased neurogenesis and improved water maze performance in comparison with uninfected control animals. Bacterial meningitis stimulated neurogenesis in the granular cell layer of the dentate gyrus: with standard housing conditions, we observed a higher density of BrdU-immunolabeled and TUC-4-expressing cells 5 weeks after induction of bacterial meningitis than in the noninfected control group. EE did not further increase progenitor cell proliferation and neuronal differentiation in the subgranular cell layer of the dentate gyrus after bacterial meningitis in comparison with infected mice housed under standard conditions. Moreover, the Morris water maze showed no significant differences between survivors of meningitis exposed to EE and animals kept in standard housing. In summary, exposure to EE after pneumococcal meningitis did not further increase meningitis-induced neurogenesis or improve spatial learning. (C) 2009 Wiley-Liss, Inc."],["dc.description.sponsorship","Else Kroner-Fresenius-Stiftung [1161/06//A70/06]"],["dc.identifier.doi","10.1002/jnr.22010"],["dc.identifier.isi","000265462800015"],["dc.identifier.pmid","19170185"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16657"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0360-4012"],["dc.title","Enriched Environment Fails To Increase Meningitis-Induced Neurogenesis and Spatial Memory in a Mouse Model of Pneumococcal Meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","865"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Infection and Immunity"],["dc.bibliographiccitation.lastpage","871"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Agarwal, Amit"],["dc.contributor.author","Tauber, Simone C."],["dc.contributor.author","Czesnik, Dirk"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Hammerschmidt, Sven"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T08:46:16Z"],["dc.date.available","2018-11-07T08:46:16Z"],["dc.date.issued","2010"],["dc.description.abstract","Toll-like receptors (TLRs) are crucial pattern recognition receptors in innate immunity that are expressed in microglia, the resident macrophages of the brain. TLR2, -4, and -9 are important in the responses against Streptococcus pneumoniae, the most common agent causing bacterial meningitis beyond the neonatal period. Murine microglial cultures were stimulated with agonists for TLR1/2 (Pam3CSK4), TLR4 (lipopolysaccharide), and TLR9 (CpG oligodeoxynucleotide) for 24 h and then exposed to either the encapsulated D39 (serotype 2) or the nonencapsulated R6 strain of S. pneumoniae. After stimulation, the levels of interleukin-6 and CCL5 (RANTES [regulated upon activation normal T-cell expressed and secreted]) were increased, confirming microglial activation. The TLR1/2, -4, and -9 agonist-stimulated microglia ingested significantly more bacteria than unstimulated cells (P < 0.05). The presence of cytochalasin D, an inhibitor of actin polymerizaton, blocked >90% of phagocytosis. Along with an increased phagocytic activity, the intracellular bacterial killing was also increased in TLR-stimulated cells compared to unstimulated cells. Together, our data suggest that microglial stimulation by these TLRs may increase the resistance of the brain against pneumococcal infections."],["dc.identifier.doi","10.1128/IAI.01110-09"],["dc.identifier.isi","000273855600033"],["dc.identifier.pmid","19933834"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20648"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0019-9567"],["dc.title","Toll-Like Receptor Stimulation Enhances Phagocytosis and Intracellular Killing of Nonencapsulated and Encapsulated Streptococcus pneumoniae by Murine Microglia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","809"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","European Journal of Endocrinology"],["dc.bibliographiccitation.lastpage","816"],["dc.bibliographiccitation.volume","143"],["dc.contributor.author","Michel, W."],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Schneider, O."],["dc.contributor.author","Shintani, Y."],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Smirnov, Alexey"],["dc.contributor.author","Stringaris, A. K."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T10:33:22Z"],["dc.date.available","2018-11-07T10:33:22Z"],["dc.date.issued","2000"],["dc.description.abstract","Objective: Follistatin (FS) is the specific binding protein of activin and expression of both factors is regulated by inflammatory agents. Therefore. FS concentrations were determined in cerebrospinal fluid (CSF) of patients with bacterial and viral meningitis or multiple sclerosis (MS), as well as in the CSF of patients without meningial inflammation or autoimmune diseases. Furthermore, a mouse pneumococcal meningitis model was used to localise the cellular sources of FS in brains of normal and meningitic mice. Methods: FS concentrations in CSF were determined by ELISA; FS in mice was localised by in situ hybridisation and immunohistochemistry. Results: FS concentrations were greater than or equal to0.4 mug/l in 22 of 66 CSF samples of meningitis patients versus 2 of 27 CSF samples from patients with multiple sclerosis (P < 0.05) and 2 of 41 CSF specimen from patients without neuroinflammatory diseases (P < 0.01). In the CSF of patients with meningitis, the concentration of FS was correlated with total protein (P < 0.005) and lactate concentrations (P < 0.05), but not with leukocyte counts, interval between onset of disease and CSF analysis, or clinical outcome. The CSF-to-serum ratios of FS and albumin also correlated significantly (P < 0.0005). in some patients with meningitis the CSF-to-serum ratios suggested that the elevated FS in CSF did not originate from serum alone. FS was localised in mice brains to neurones of the hippocampus, dentate gyrus, neocortex, and to the choroid plexus. Analyses of brains and other organs from uninfected and infected animals sacrificed 6-36 h after infection did not reveal any obvious differences in the distribution and intensity of FS mRNA and protein expression. Conclusions: The concentration of FS in humans is elevated during meningitis. In some patients the increase is caused by a release of FS from brain into CSF. Data from the mouse meningitis model suggest that increased CSF concentrations of FS in meningitis appear not to be accompanied by an elevated number of cells containing FS mRNA or protein in the brain."],["dc.identifier.isi","000166654700013"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44594"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bioscientifica Ltd"],["dc.relation.issn","0804-4643"],["dc.title","Follistatin (FS) in human cerebrospinal fluid and regulation of FS expression in a mouse model of meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","289"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","298"],["dc.bibliographiccitation.volume","94"],["dc.contributor.author","Lotz, M."],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Iliev, Asparouh I."],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Wiazewicz, N."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T09:20:41Z"],["dc.date.available","2018-11-07T09:20:41Z"],["dc.date.issued","2005"],["dc.description.abstract","The interaction of endogenous and exogenous stimulators of innate immunity was examined in primary cultures of mouse microglial cells and macrophages after application of defined Toll-like receptor (TLR) agonists [lipopolysaccharide (LPS) (TLR4), the synthetic lipopeptide Pam3Cys-Ser-Lys4 (Pam3Cys) (TLR2) and single-stranded unmethylated CpG-DNA (CpG) (TLR9)] alone and in combination with amyloid beta peptide (Abeta) 1-40. Abeta 1-40 stimulated microglial cells and macrophages primed by interferon-gamma in a dose-dependent manner. Co-administration of Abeta1-40 with LPS or Pam3Cys led to an additive release of nitric oxide (NO) and tumour necrosis factor alpha (TNF-alpha). This may be one reason for the clinical deterioration frequently observed in patients with Alzheimer's disease during infections. In contrast, co-application of Abeta1-40 with CpG led to a substantial decrease of NO and TNF- alpha release compared with stimulation with CpG alone. Abeta 1-40 and CpG did not co-localize within the same subcellular compartment, making a direct physicochemical interaction as the cause of the observed antagonism very unlikely. This suggests that not all TLR agonists enhance the stimulatory effect of Abeta on innate immunity."],["dc.identifier.doi","10.1111/j.1471-4159.2005.03188.x"],["dc.identifier.isi","000230289200001"],["dc.identifier.pmid","15998280"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28935"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1471-4159"],["dc.relation.issn","0022-3042"],["dc.title","Amyloid beta peptide 1-40 enhances the action of Toll-like receptor-2 and -4 agonists but antagonizes Toll-like receptor-9-induced inflammation in primary mouse microglial cell cultures"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","87"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","96"],["dc.bibliographiccitation.volume","159"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Bader, Samuel"],["dc.contributor.author","Muhlhauser, F."],["dc.contributor.author","Brechtel, K."],["dc.contributor.author","Mitchell, Timothy J."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T08:28:47Z"],["dc.date.available","2018-11-07T08:28:47Z"],["dc.date.issued","2005"],["dc.description.abstract","Microglial cells express Toll-like receptors (TLRs) recognising exogenous and endogenous ligands. Upon stimulation with agonists of TLR2, TLR4, and TLR9, nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) were released by primary mouse microglial cell cultures. Endotoxin was most potent in stimulating microglia followed by pneumolysin, cytosine-guanosine (CpG) oligodesoxynucleotide (ODN), and Tripalmitoyl-S-glycetyl-cysteine. Maximum stimulation of TLR2, TLR4, and TLR9 resulted in approximately equal amounts of nitric oxide release. Pneumolysin was a potent activator of microglial cells; at high concentrations, it reduced cell viability. No cytotoxicity was noted with the other TLR agonists. Costimulation with maximum concentrations of two TLR agonists did not further increase nitric oxide release. Costimulation with submaximum concentrations was additive or supraadditive, suggesting that even low concentrations of products of infectious agents can lead to microglial activation via TLRs. (C) 2004 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneuroim.2004.10.005"],["dc.identifier.isi","000226882300010"],["dc.identifier.pmid","15652406"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16503"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1872-8421"],["dc.relation.issn","0165-5728"],["dc.title","Dose-dependent activation of microglial cells by Toll-like receptor agonists alone and in combination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","228"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Loleit, Tobias"],["dc.contributor.author","Zeretzke, Moritz"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T08:36:51Z"],["dc.date.available","2018-11-07T08:36:51Z"],["dc.date.issued","2010"],["dc.identifier.isi","000283694400048"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18406"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","10th Congress of the International-Society-of-Neuroimmunology (ISNI)"],["dc.relation.eventlocation","Sitges, SPAIN"],["dc.title","Additive microglial-mediated neuronal injury induced by Amyloid-beta and bacterial TLR agonists"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","367"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","376"],["dc.bibliographiccitation.volume","58"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Czesnik, Dirk"],["dc.contributor.author","Scheffel, Joerg"],["dc.contributor.author","Zeug, Andre"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Hammerschmidt, Sven"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T08:46:15Z"],["dc.date.available","2018-11-07T08:46:15Z"],["dc.date.issued","2010"],["dc.description.abstract","Microglia express Toll-like receptors (TLRs) that recognize invading pathogens as well as endogenous proteins such as fibronectin under nonphysiological conditions. Here, we demonstrated that fibronectin stimulates murine microglia in culture in a dose-dependent manner: microglial cells secreted proinflammatory cytokines and chemokines and increased phagocytosis of Escherichia coli DH5 alpha and E. coli K1 strains. Low levels of fibronectin exerted a synergistic effect on the release of proinflammatory compounds by microglia co-stimulated with agonists for TLR1/2 (Pam(3)CSK(4)) or TLR9 (CpG DNA), but not in combination with the TLR4 agonist lipopolysaccharide (LPS). Phagocytosis of bacterial strains was moderately enhanced when microglia was co-stimulated with high concentrations of fibronectin and one pathogen-derived TLR agonist. In conclusion, fibronectin increased proinflammatory and phagocytotic functions in microglia and partially synergized with microbial TLR agonists. (C) 2009 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/glia.20929"],["dc.identifier.isi","000273189600009"],["dc.identifier.pmid","19780198"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20644"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0894-1491"],["dc.title","Fibronectin Stimulates Escherichia coli Phagocytosis by Microglial Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","559"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","European Journal of Endocrinology"],["dc.bibliographiccitation.lastpage","564"],["dc.bibliographiccitation.volume","148"],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Phillips, D."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T10:39:07Z"],["dc.date.available","2018-11-07T10:39:07Z"],["dc.date.issued","2003"],["dc.description.abstract","Objective: Activin is a growth and differentiation factor of many cell types, and has recently been implicated in inflammatory processes. Clinical data linking activin and its binding protein, follistatin (FS), are lacking. We measured serum levels of activin and FS in patients diagnosed with septicemia. Patients and measurements: Eight male and seven female patients of different ages, various forms of septicemia and different clinical outcome were investigated and compared with age- and sex-matched healthy controls. Serum concentrations of FS, activin, C-reactive protein (CRP) and blood leukocyte counts were determined during septicemia. Results: The median of the maximum activin concentrations of septicemic patients was 3.9-fold higher than in age- and sex-matched healthy control subjects (P < 0.01); the median of the maximum FS concentrations was 2.6-fold higher (P < 0.01). The highest increase of activin in septicemic patients was approximately 15.8-fold, whereas FS increased by up to 13.2-fold above normal. FS, activin and CRP serum levels generally paralleled each other, but were not correlated with leukocyte counts or clinical outcome. Conclusions: Circulatory concentrations of activin and FS are elevated in patients diagnosed with septicemia, consistent with potential roles in the systemic inflammatory response."],["dc.identifier.doi","10.1530/eje.0.1480559"],["dc.identifier.isi","000182915600012"],["dc.identifier.pmid","12720540"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45971"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bio Scientifica Ltd"],["dc.relation.issn","0804-4643"],["dc.title","Serum concentrations of activin and follistatin are elevated and run in parallel in patients with septicemia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S20"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","S21"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T08:51:34Z"],["dc.date.available","2018-11-07T08:51:34Z"],["dc.date.issued","2011"],["dc.identifier.isi","000294178900077"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21966"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Malden"],["dc.relation.issn","0894-1491"],["dc.title","PHAGOCYTOSIS OF PATHOGENS BY STIMULATED MURINE MICROGLIA"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1124"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Neuroscience Research"],["dc.bibliographiccitation.lastpage","1136"],["dc.bibliographiccitation.volume","88"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Goos, Miriam"],["dc.contributor.author","Rollwagen, Lena"],["dc.contributor.author","Baake, Daniel"],["dc.contributor.author","Zech, Wolf-Dieter"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Schliebs, Reinhard"],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2018-11-07T08:44:39Z"],["dc.date.available","2018-11-07T08:44:39Z"],["dc.date.issued","2010"],["dc.description.abstract","Neurological symptoms of patients suffering from neurodegenerative diseases such as Alzheimer's dementia (AD), Parkinson's disease (PD), or amyotrophic lateral sclerosis (ALS) often worsen during infections. We assessed the disease-modulating effects of recurrent systemic infections with the most frequent respiratory pathogen, Streptococcus pneumoniae, on the course of AD, PD, and ALS in mouse models of these neurodegenerative diseases [transgenic Tg2576 mice, (Thy1)-[A30P]alpha SYN mice, and Tg(SOD1-G93A) mice]. Mice were repeatedly challenged intraperitoneally with live S. pneumoniae type 3 and treated with ceftriaxone for 3 days. Infection caused an increase of interleukin-6 concentrations in brain homogenates. The clinical status of (Thy1)-[A30P]alpha SYN mice and Tg(SOD1-G93A) mice was monitored by repeated assessment with a clinical score. Motor performance was controlled by the tightrope test and the rotarod test. In Tg2576 mice, spatial memory and learning deficits were assessed in the Morris water maze. In none of the three mouse models onset or course of the disease as evaluated by the clinical tests was affected by the recurrent systemic infections performed. Levels of a-synuclein in brains of (Thy1)-[A30P]alpha SYN mice did not differ between infected animals and control animals. Plaque sizes and concentrations of A beta 1-40 and A beta 1-42 were not significantly different in brains of infected and uninfected Tg2576 mice. In conclusion, onset and course of disease in mouse models of three common neurodegenerative disorders were not influenced by repeated systemic infections with S. pneumoniae, indicating that the effect of moderately severe acute infections on the course of neurodegenerative diseases may be less pronounced than suspected. (C) 2009 Wiley-Liss, Inc."],["dc.description.sponsorship","Else Kroner-Fresenius-Stiftung [P35/05//A46/05]"],["dc.identifier.doi","10.1002/jnr.22270"],["dc.identifier.isi","000275583200020"],["dc.identifier.pmid","19859962"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20250"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0360-4012"],["dc.title","Recurrent Systemic Infections With Streptococcus pneumoniae Do Not Aggravate the Course of Experimental Neurodegenerative Diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]