Research Topics
| Clive BateSummaryAffiliation: Royal Veterinary College Country: UK Publications
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Publications
Temporal and spatial relationship between the death of PrP-damaged neurones and microglial activationClive Bate
Institute of Comparative Medicine, Department of Veterinary Pathology, Univeristy of Glasgow Veterinary School, Bearsden Road, Glasgow G61 IQH, UK
Neuroreport 13:1695-700. 2002..Activation of microglia and microglia-mediated killing of PrP-treated neurones or scrapie-infected neuroblastoma cells were maximal only when microglia were in direct contact with neurones...
Docosahexaenoic and eicosapentaenoic acids increase neuronal death in response to HuPrP82-146 and Abeta 1-42Clive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, AL9 7TA North Mymms, Herts, UK
Neuropharmacology 54:934-43. 2008..Such observations raise the possibility that some PUFA supplements may accelerate neuronal loss in the terminal stages of prion or Alzheimer's diseases...
Cholesterol esterification reduces the neurotoxicity of prionsClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Hatfield, Hertfordshire AL9 7TA, UK
Neuropharmacology 54:1247-53. 2008..These results indicate that cholesterol esterification is an important cellular response that reduces PrP(Sc)-induced activation of PLA(2) and protects against cell death in ScGT1 cells...
Docosahexaenoic and eicosapentaenoic acids increase prion formation in neuronal cellsClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Herts, UK, AL9 7TA
BMC Biol 6:39. 2008..Since polyunsaturated fatty acids also reduced cellular cholesterol levels we tested their effects on PrPSc formation in three prion-infected neuronal cell lines (ScGT1, ScN2a and SMB cells)...
Polyunsaturated fatty acids protect against prion-mediated synapse damage in vitroClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, North Mymms, Herts, AL9 7TA, UK
Neurotox Res 17:203-14. 2010..Such observations raise the possibility that supplements containing PUFA may protect against the synapse damage and cognitive loss seen during the early stages of prion diseases...
Clustering of sialylated glycosylphosphatidylinositol anchors mediates PrP-induced activation of cytoplasmic phospholipase A 2 and synapse damageClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Herts, UK
Prion 6:350-3. 2012....
Neurodegeneration induced by clustering of sialylated glycosylphosphatidylinositols of prion proteinsClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Hatfield, Hertfordshire AL9 7TA, United Kingdom
J Biol Chem 287:7935-44. 2012....
Squalestatin alters the intracellular trafficking of a neurotoxic prion peptideRona Wilson
1Division of Immunology, Infection and Inflammation, Western Infirmary, University of Glasgow, G11 6NT, Glasgow
BMC Neurosci 8:99. 2007....
Platelet-activating factor antagonists protect amyloid-beta damaged neurons from microglia-mediated deathClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Hatfield, Hertfordshire AL9 7TA, UK
Neuropharmacology 51:173-81. 2006..At nanomolar concentrations PAF induces a change in neuronal phenotype that activates microglia via the CD14 molecule, these activated microglia then kill the amyloid-beta1-42 damaged neurons...
Cholesterol synthesis inhibitors protect against platelet-activating factor-induced neuronal damageClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, North Mymms, Herts, UK
J Neuroinflammation 4:5. 2007..Since some epidemiological studies demonstrate that statins, drugs that reduce cholesterol synthesis, have a beneficial effect on mild AD, we examined the effects of two cholesterol synthesis inhibitors on neuronal responses to PAF...
Squalestatin protects neurons and reduces the activation of cytoplasmic phospholipase A2 by Abeta(1-42)Clive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Herts AL9 7TA, UK
Neuropharmacology 53:222-31. 2007..This process is dependent on the amounts of cholesterol in neuronal membranes and is susceptible to treatment with squalestatin or simvastatin...
Ginkgolides protect against amyloid-beta1-42-mediated synapse damage in vitroClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Herts, AL9 7TA, UK
Mol Neurodegener 3:1. 2008....
Sequestration of free cholesterol in cell membranes by prions correlates with cytoplasmic phospholipase A2 activationClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Herts, AL9 7TA, UK
BMC Biol 6:8. 2008....
Prostaglandin D2 mediates neuronal damage by amyloid-beta or prions which activates microglial cellsClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Herts, AL9 7TA, UK
Neuropharmacology 50:229-37. 2006....
Microglial cells kill prion-damaged neurons in vitro by a CD14-dependent processClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Herts AL9 7TA, UK
J Neuroimmunol 170:62-70. 2005..None of the mabs affected the survival of HuPrP106-126-damaged neurons in the absence of monocytes...
Amyloid-β-induced synapse damage is mediated via cross-linkage of cellular prion proteinsClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Hertfordshire AL9 7TA, United Kingdom
J Biol Chem 286:37955-63. 2011..This hypothesis was supported by our observation that monoclonal antibody mediated cross-linkage of PrP(C) also activated synaptic cPLA(2) and caused synapse damage...
Monoacylated cellular prion protein modifies cell membranes, inhibits cell signaling, and reduces prion formationClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Hertfordshire AL9 7TA, United Kingdom
J Biol Chem 286:8752-8. 2011..In addition, our observations raise the possibility that pharmacological modification of GPI anchors might constitute a novel therapeutic approach to prion diseases...
α-synuclein induced synapse damage is enhanced by amyloid-β1-42Clive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Herts, AL9 7TA, UK
Mol Neurodegener 5:55. 2010....
Amyloid-β(1-40) inhibits amyloid-β(1-42) induced activation of cytoplasmic phospholipase A2 and synapse degenerationClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, North Mymms, Herts, UK
J Alzheimers Dis 21:985-93. 2010..Such observations raise the possibility that the amount of Aβ(1-40) produced within the brain is critical in determining the synapse damaging effects of Aβ(1-42) and possibly the cognitive loss seen during the early stages of AD...
A glycosylphosphatidylinositol analogue reduced prion-derived peptide mediated activation of cytoplasmic phospholipase A2, synapse degeneration and neuronal deathClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, North Mymms, Herts, UK
Neuropharmacology 59:93-9. 2010..We conclude that glucosamine-PI, or isolated GPI anchors, can modify local membrane micro-environments that are important in the initiation of signalling events that mediate PrP82-146 induced neurodegeneration...
Phospholipase A2 inhibitors protect against prion and Abeta mediated synapse degenerationClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Herts, AL9 7TA, UK
Mol Neurodegener 5:13. 2010..A pharmacological approach was used to screen cell signalling pathways involved in synapse degeneration...
The glycosylphosphatidylinositol anchor is a major determinant of prion binding and replicationClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Herts AL9 7TA, UK
Biochem J 428:95-101. 2010..We conclude that the nature of the GPI anchor attached to PrPSc affected the binding of PrPSc to neurons, its localization to lipid rafts and its ability to convert endogenous PrPC...
Glimepiride reduces the expression of PrPc, prevents PrPSc formation and protects against prion mediated neurotoxicity in cell linesClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, North Mymms, United Kingdom
PLoS ONE 4:e8221. 2009..The accumulation of PrP(Sc) within the brain is associated with synapse loss and ultimately neuronal death. Novel therapeutics are desperately required to treat neurodegenerative diseases including the prion diseases...
Ethanol protects cultured neurons against amyloid-β and α-synuclein-induced synapse damageClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Herts AL9 7TA, UK
Neuropharmacology 61:1406-12. 2011..These results may help explain epidemiological reports that moderate alcohol consumption protects against the development of dementia in Alzheimer's and Parkinson's diseases...
PrP-specific camel antibodies with the ability to immunodetect intracellular prion proteinMourad Tayebi
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Hatfield, Hertfordshire AL9 7TA, UK
J Gen Virol 91:2121-31. 2010....
The cellular prion protein with a monoacylated glycosylphosphatidylinositol anchor modifies cell membranes, inhibits cell signaling and reduces prion formationClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, North Mymms, Herts, UK on protein PrP
Prion 5:65-8. 2011..In addition, such observations raise the possibility that the pharmacological modification of GPI anchors might constitute a novel therapeutic approach to prion diseases...
Glycosylphosphatidylinositol anchor analogues sequester cholesterol and reduce prion formationClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Herts AL9 7TA, United Kingdom
J Biol Chem 285:22017-26. 2010..We propose that treatment with glucosamine-PI modifies local micro-environments that control PrP(C) expression and activation of PLA(2) and subsequently inhibits PrP(Sc) formation...
A camelid anti-PrP antibody abrogates PrP replication in prion-permissive neuroblastoma cell linesDaryl Rhys Jones
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hertfordshire, United Kingdom
PLoS ONE 5:e9804. 2010..These findings demonstrate the potential use of anti-prion camelid antibodies for the treatment of prion and other related diseases via non-invasive means...
Inhibition of phospholipase A2 increased the removal of the prion derived peptide PrP82-146 from cultured neuronsClive Bate
Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Herts AL9 7TA, UK
Neuropharmacology 60:365-72. 2011..We conclude that activation of PLA(2) and the production of PAF control a cholesterol-sensitive pathway that affects the cellular localisation and hence the fate of PrP82-146 in neurons...
A role for B lymphocytes in anti-infective prion therapies?Mourad Tayebi
Department of Pathology and Infectious Diseases, The Royal Veterinary College, North Mymms, Hatfield, Hertfordshire, UK
Expert Rev Anti Infect Ther 5:631-8. 2007..Furthermore, in vivo stimulation of immune-competent cells to specifically recognize and neutralize the abnormally folded isoform should also be pursued...
Cyclo-oxygenase inhibitors protect against prion-induced neurotoxicity in vitroClive Bate
Institute of Comparative Medicine, Glasglow University Veterinary School, Glasgow, UK
Neuroreport 13:1933-8. 2002..The cox-1 inhibitors also inhibited neuronal PGE production and protected both neuroblastoma cells and primary cortical neurones against prions. They also reduced microglia-mediated killing of prion-treated neurones...
Neurones treated with cyclo-oxygenase-1 inhibitors are resistant to amyloid-beta1-42Clive Bate
Institute of Comparative Medicine, Department of Veterinary Pathology, Glasgow University Veterinary School, Bearsden Road, Glasgow G61 1QH, UK
Neuroreport 14:2099-103. 2003..Although the production of neuronal prostaglandin E2 in response to amyloid-beta1-42 was reduced by the presence of COX-1 inhibitors, no neurotoxic effects of prostaglandin E2, or any other prostaglandin, were observed...
Simvastatin treatment prolongs the survival of scrapie-infected miceSarah Kempster
Department of Obstetrics and Gynaecology, University of Cambridge, Rosie Hospital, Robinson Way, Cambridge, UK
Neuroreport 18:479-82. 2007..183 days). These results indicate that low-dosage simvastatin treatment affects the progression of experimental scrapie, and supports the concept that statin treatment may influence the prion pathogenesis...
Squalestatin cures prion-infected neurons and protects against prion neurotoxicityClive Bate
Institute of Comparative Medicine, Department of Veterinary Pathology, University of Glasgow Veterinary School, Bearsden Road, Glasgow G61 1QH, United Kingdom
J Biol Chem 279:14983-90. 2004..These studies indicate a pivotal role for cholesterol-sensitive processes in controlling PrP(Sc) formation, and in the activation of signaling pathways associated with PrP-induced neuronal death...
The role of platelet activating factor in prion and amyloid-beta neurotoxicityClive Bate
Department of Veterinary Pathology, Glasgow University Veterinary School, Bearsden Road, Glasgow G61 1QH, UK
Neuroreport 15:509-13. 2004....
Microglia kill amyloid-beta1-42 damaged neurons by a CD14-dependent processClive Bate
Institute of Comparative Medicine, Department of Veterinary Pathology, Glasgow University Veterinary School, Bearsden Road, Glasgow G61 1QH, UK
Neuroreport 15:1427-30. 2004..These results indicate an important role for CD14 in the recognition and subsequent killing of amyloid-beta damaged neurons by microglia...
Detoxified lipopolysaccharide reduces microglial cell killing of prion-infected neuronsClive Bate
Department of Veterinary Pathology, Glasgow University Veterinary School, Bearsden Road, Glasgow G61 1QH, UK
Neuroreport 15:2765-8. 2004..These results suggest that some compounds that bind to CD14 might reduce microglial cell activation and increase neuronal survival in prion and Alzheimer's diseases...
Phospholipase A2 inhibitors or platelet-activating factor antagonists prevent prion replicationClive Bate
Department of Veterinary Pathology, Glasgow University Veterinary School, Bearsden Road, Glasgow G61 1QH, Scotland, United Kingdom
J Biol Chem 279:36405-11. 2004..These data indicate a pivotal role for PLA(2) and PAF in controlling PrP(res) formation and identify them as potential therapeutic agents...
Role of glycosylphosphatidylinositols in the activation of phospholipase A2 and the neurotoxicity of prionsClive Bate
Department of Veterinary Pathology, Glasgow University Veterinary School, Bearsden Road, Glasgow G61 1QH, UK
J Gen Virol 85:3797-804. 2004..These results implicate phospholipase A(2) activation by PrP-GPIs as an early event in prion-induced neurodegeneration...
Manipulation of PrPres production in scrapie-infected neuroblastoma cellsClive Bate
Department of Veterinary Pathology, Institute of Comparative Medicine, University of Glasgow Veterinary School, Bearsden Road, Glasgow G61 1QH, UK
J Neurosci Methods 138:217-23. 2004..The production of interleukin-6 by microglia cultured with retinoic acid-treated ScN2a cells was significantly higher than that of microglia cultured with untreated ScN2a cells...
