... utility of anti-inflammatory drugtherapies in the treatment of AD.Microglia are the principle immune effector cells in the brain and represent approximately 5–10% of all gliafound in the brain. ... purposes)Journal of NeuroinflammationOpen AccessReviewThe microglial NADPH oxidase complex as a source ofoxidative stress in Alzheimer& apos;s disease Brandy L Wilkinson* and Gary E LandrethAddress: Alzheimer ... complex leads to theinitiation of complex signaling events leading to proteintyrosine phosphorylation and activation of the src-familykinases Lyn and Fyn as well as the tyrosine kinase Syk[30,32,52]....
... synthase. The increased activities of argininosuccinate synthetase and argininosuccinate lyase suggest the increased and effective recycling of citrulline to arginine in anoxia, making nitric ... findings of NO involvement in pathophysiol-ogy of hypobaric hypoxia inbrain (42-43). In this study the increased activity of NOS in anoxia may represent predominantly the nNOS form. In inflam-matory ... the way of competing NOS for arginine. In a recent study using GS inhibitor, it is showed a reduced concentration of glutamine and glutamate in brain due to GS inhibition (56). The sustained...
... a subset of NSAIDs(e.g. ibuprofen, flurbiprofen, indomethacin) reduced brain inflammation and Aβ levels in addition to the dep-osition of Aβ inbrain [13,14]. Despite this evidence, and the ... that a full dose of indomethacin alone despite a significant reduction in brain inflammation had only a marginal effect on brain oxidative stressin the Tg2576 mice [16]. This finding sug-gests ... CentralPage 1 of 9(page number not for citation purposes)Journal of NeuroinflammationOpen AccessResearch Brain inflammation andoxidativestressin a transgenic mouse model of Alzheimer- like brain...
... determine theeffects of Hsp105a on JNK and p38 signalling pathways, weexamined the activation of JNK and p38 in F9 cells by oxidative stress. As shown in Fig. 6A, JNK was notactivated in control ... activation of p38 induced by oxidative stress, we further examined whether its activationis responsible for the induction of apoptosis in F9 cells usingSB202190, a potent inhibitor of p38. As shown in ... peroxide. In contrast, hydrogen peroxide-treat-ment induced marked activation of JNK within 30 min in S23 cells, but not in S3 cells. Therefore, the enhancement of the oxidative stress- induced...
... calciumtransients during reversible brain ischemia. Exp Brain Res 104, 462–466.188 Silver IA & Erecinska M (1992) Ion homeostasis in rat brain in vivo: intra- and extracellular [Ca2+] and [H+ ]in the ... by proteins resi-ding in both the inner and outer mitochondrialmembrane, that is activated by mitochondrial Ca2+overloading and other factors including oxidative stress [88,89]. In neurons ... imposing a continuous load of calcium to the neuron. The turning point upon whichthe cell looses the ability to buffer the incoming calciumresulting in an abrupt, sustained and irreversibleincrease...
... PARP inhibitor, on oxidative stress- induced changes in D. discoideum development. Interestingly, oxidativestress resulted in PARPactivation within 5 min that was inhibited by benzamide. Oxidative ... development.HA-induced oxidativestress activates PARP within5 min (Fig. 4A,B), and its role during oxidative stress is further confirmed by the use of low concentrations of benzamide. Preincubation of cells ... the response of this organism to oxidative stress and the role of PARP during development. We used hydroxylamine (HA)to induce in situ generation of H2O2 and monitored the effect of benzamide,...
... cellactivity of several LOX inhibitors, including aesculetin (anonselective LOX inhibitor), MK886 (an inhibitor of the5-LOX-activating protein), zileuton (a 5-LOX inhibitor),baicalein (a 12/15-LOX inhibitor), ... leads to inactivation of MKPs and activation of MAPKs [7-9]. ROS-mediatedinhibition of MKPs is critical for TNFα-induced sus-tained activation of JNK and subsequent apoptosis [7].Interestingly, ... [11,12], and pro-mote apoptosis. In fact, ROS-induced oxidative stress and cell death play important roles in the efficacy of manyantineoplastic agents [13,14].To investigate whether oxidative stress...
... in Alzheimer brain. Brain Res 1997, 769:391-395.79. Walker DG, McGeer PL: Complement gene expression in human brain: comparison between normal and Alzheimer disease cases. Brain Res Mol Brain ... proteins including CD59, clus-terin, vitronectin, C1-inhibitor, C4-binding protein,decay-activating factor, and Factor H, which inhibit differ-ent steps in the complement cascade. All of these ... theremoval of microorganisms and the processing of immune complexes. Numerous studies haveprovided evidence for an increase in this process in areas of pathology in the Alzheimer& apos;s disease (AD) brain. ...
... study, we examined brain tissue from cases ofAlzheimerdisease for the presence of BRCA1, a known regulator of cell cycle, and found intense and specific localization of BRCA1 to neurofibrillary ... in all cases ofAlzheimer disease. These findings not only further define the cell cycle reentry phenotype inAlzheimer disease but also indicate that the neurofibrillary tangles which define ... up-regulation of nitro-tyrosine in Alzheimer& apos;s disease brain. Brain Res 1997; 774: 193-9. 18. Mecocci P, MacGarvey U, Beal MF. Oxidative damage to mito-chondrial DNA is increased in Alzheimer& apos;s...
... pilocarpine, on muscarinic and dopaminer-gic receptors and on phosphoinositide metabolism in rat hippocampus and striatum. Neurochem Int 33,299–306.21 Viana GSB, Marinho MMF, Sousa FCF, Bruin VMS,Aguiar ... nitrate and H2O2,are normally produced in the brain. H2O2is convertedinto water by catalase and glutathione peroxidase,which involves GSH, a cofactor of this enzyme [5,8].GSH is one of ... findings show that pilocarpine induces SE,which can produce alterations in superoxide dismutase and catalase activities in different areas, thereby pro-tecting the brain from neuronal damage induced...