V H Perry

Summary

Affiliation: University of Southampton
Country: UK

Publications

  1. ncbi Innate inflammation in Parkinson's disease
    V Hugh Perry
    School of Biological Sciences, University of Southampton, Southampton, UK
    Cold Spring Harb Perspect Med 2:a009373. 2012
  2. ncbi Axon damage and repair in multiple sclerosis
    V H Perry
    Central Nervous System Inflammation Group, School of Biological Sciences, University of Southampton, UK
    Philos Trans R Soc Lond B Biol Sci 354:1641-7. 1999
  3. ncbi Stress primes microglia to the presence of systemic inflammation: implications for environmental influences on the brain
    V Hugh Perry
    CNS Inflammation Group, School of Biological Sciences, University of Southampton, Southampton SO16 7PX, UK
    Brain Behav Immun 21:45-6. 2007
  4. ncbi The impact of systemic infection on the progression of neurodegenerative disease
    V Hugh Perry
    CNS Inflammation Group, School of Biological Sciences, University of Southampton, Southampton SO16 7PX, UK
    Nat Rev Neurosci 4:103-12. 2003
  5. ncbi Systemic infections and inflammation affect chronic neurodegeneration
    V Hugh Perry
    Southampton Neuroscience Group, School of Biological Sciences and School of Medicine, University of Southampton, Southampton SO16 7PX, UK
    Nat Rev Immunol 7:161-7. 2007
  6. ncbi C1q: the perfect complement for a synaptic feast?
    V Hugh Perry
    School of Biological Sciences, University of Southampton, Southampton, SO16 7PX, UK
    Nat Rev Neurosci 9:807-11. 2008
  7. ncbi Atypical inflammation in the central nervous system in prion disease
    V Hugh Perry
    CNS Inflammation Group, School of Biological Sciences, University of Southampton, Southampton SO16 7PX, UK
    Curr Opin Neurol 15:349-54. 2002
  8. ncbi The influence of systemic inflammation on inflammation in the brain: implications for chronic neurodegenerative disease
    V Hugh Perry
    CNS Inflammation Group, University of Southampton, Biomedical Sciences Building, Southampton SO16 7PX, UK
    Brain Behav Immun 18:407-13. 2004
  9. ncbi The role of microglia in synaptic stripping and synaptic degeneration: a revised perspective
    V Hugh Perry
    School of Biological Sciences, University of Southampton, Southampton, U K
    ASN Neuro 2:e00047. 2010
  10. ncbi Contribution of systemic inflammation to chronic neurodegeneration
    V Hugh Perry
    School of Biological Sciences, University of Southampton, Southampton General Hospital, Southampton SO16 6YD, UK
    Acta Neuropathol 120:277-86. 2010

Collaborators

Detail Information

Publications74

  1. ncbi Innate inflammation in Parkinson's disease
    V Hugh Perry
    School of Biological Sciences, University of Southampton, Southampton, UK
    Cold Spring Harb Perspect Med 2:a009373. 2012
    ....
  2. ncbi Axon damage and repair in multiple sclerosis
    V H Perry
    Central Nervous System Inflammation Group, School of Biological Sciences, University of Southampton, UK
    Philos Trans R Soc Lond B Biol Sci 354:1641-7. 1999
    ..The presence of early axon injury and the consequences of an ever increasing load of neuronal damage has important implications not only for when therapy should be initiated in MS but also the therapeutic target...
  3. ncbi Stress primes microglia to the presence of systemic inflammation: implications for environmental influences on the brain
    V Hugh Perry
    CNS Inflammation Group, School of Biological Sciences, University of Southampton, Southampton SO16 7PX, UK
    Brain Behav Immun 21:45-6. 2007
  4. ncbi The impact of systemic infection on the progression of neurodegenerative disease
    V Hugh Perry
    CNS Inflammation Group, School of Biological Sciences, University of Southampton, Southampton SO16 7PX, UK
    Nat Rev Neurosci 4:103-12. 2003
  5. ncbi Systemic infections and inflammation affect chronic neurodegeneration
    V Hugh Perry
    Southampton Neuroscience Group, School of Biological Sciences and School of Medicine, University of Southampton, Southampton SO16 7PX, UK
    Nat Rev Immunol 7:161-7. 2007
    ....
  6. ncbi C1q: the perfect complement for a synaptic feast?
    V Hugh Perry
    School of Biological Sciences, University of Southampton, Southampton, SO16 7PX, UK
    Nat Rev Neurosci 9:807-11. 2008
    ....
  7. ncbi Atypical inflammation in the central nervous system in prion disease
    V Hugh Perry
    CNS Inflammation Group, School of Biological Sciences, University of Southampton, Southampton SO16 7PX, UK
    Curr Opin Neurol 15:349-54. 2002
    ..There is also now evidence to suggest that a peripheral infection, and its consequent systemic cytokine expression, may drive central nervous system cytokine expression and perhaps exacerbate disease...
  8. ncbi The influence of systemic inflammation on inflammation in the brain: implications for chronic neurodegenerative disease
    V Hugh Perry
    CNS Inflammation Group, University of Southampton, Biomedical Sciences Building, Southampton SO16 7PX, UK
    Brain Behav Immun 18:407-13. 2004
    ..These interactions suggest that systemic infections, or indeed any systemic challenge that promotes a systemic inflammatory response, may contribute to the outcome or progression of chronic neurodegenerative disease...
  9. ncbi The role of microglia in synaptic stripping and synaptic degeneration: a revised perspective
    V Hugh Perry
    School of Biological Sciences, University of Southampton, Southampton, U K
    ASN Neuro 2:e00047. 2010
    ..We highlight here some of the gaps in our understanding of synapse degeneration in chronic neurodegenerative disease...
  10. ncbi Contribution of systemic inflammation to chronic neurodegeneration
    V Hugh Perry
    School of Biological Sciences, University of Southampton, Southampton General Hospital, Southampton SO16 6YD, UK
    Acta Neuropathol 120:277-86. 2010
    ....
  11. ncbi MCP-1 and murine prion disease: separation of early behavioural dysfunction from overt clinical disease
    L M Felton
    CNS Inflammation Group, School of Biological Sciences, University of Southampton, Southampton, SO16 7PX, UK
    Neurobiol Dis 20:283-95. 2005
    ....
  12. ncbi Neuropathologically distinct prion strains give rise to similar temporal profiles of behavioral deficits
    C Cunningham
    CNS Inflammation Group, Southampton Neurosciences Group, School of Biological Sciences, Bassett Crescent East, Southampton, SO16 7PX, UK
    Neurobiol Dis 18:258-69. 2005
    ..These behavioral similarities coupled with clear pathological differences could serve to identify key circuits whose early dysfunction underlies the neurological effects of different prion strains...
  13. ncbi The effect of non-steroidal anti-inflammatory agents on behavioural changes and cytokine production following systemic inflammation: Implications for a role of COX-1
    J L Teeling
    CNS Inflammation Group, School of Biological Sciences, University of Southampton, Bassett Crescent East SO167PX, UK
    Brain Behav Immun 24:409-19. 2010
    ..Our results may have implications for novel therapeutic strategies to treat or prevent neurological diseases with an inflammatory component...
  14. ncbi Brain cytokine synthesis induced by an intraparenchymal injection of LPS is reduced in MCP-1-deficient mice prior to leucocyte recruitment
    E L Rankine
    Nurin Ltd, School of Biological Sciences, University of Southampton, Southampton, SO16 7PX, UK
    Eur J Neurosci 24:77-86. 2006
    ....
  15. ncbi T-cell- and macrophage-mediated axon damage in the absence of a CNS-specific immune response: involvement of metalloproteinases
    T A Newman
    CNS Inflammation Group, School of Biological Sciences, University of Southampton, UK
    Brain 124:2203-14. 2001
    ..Our results show that axon injury, possibly mediated by MMPs, is immunologically non-specific and may continue behind an intact blood-brain barrier...
  16. ncbi Sub-pyrogenic systemic inflammation impacts on brain and behavior, independent of cytokines
    J L Teeling
    CNS Inflammation Group, School of Biological Sciences, University of Southampton, Bassett Crescent East, UK
    Brain Behav Immun 21:836-50. 2007
    ..Taken together, these experiments suggest a key role for prostaglandins, rather than cytokines, in communicating to the brain...
  17. ncbi Alpha-synuclein deficiency in the C57BL/6JOlaHsd strain does not modify disease progression in the ME7-model of prion disease
    A A Asuni
    CNS Inflammation Group, University of Southampton, UK
    Neuroscience 165:662-74. 2010
    ..Our data suggest that alpha-synuclein deficiency does not contribute to the compartment specific processes that give rise to prion disease mediated synaptotoxicity and neurodegeneration...
  18. ncbi Systemic inflammation and disease progression in Alzheimer disease
    C Holmes
    Clinical Neurosciences Division, University of Southampton, UK
    Neurology 73:768-74. 2009
    ..Previous preclinical research shows that acute systemic inflammation contributes to an exacerbation of neurodegeneration by activation of primed microglial cells...
  19. ncbi Systemic inflammation switches the inflammatory cytokine profile in CNS Wallerian degeneration
    Karine Palin
    CNS Inflammation Group, School of Biological Sciences, University of Southampton, Southampton SO16 7PX, UK
    Neurobiol Dis 30:19-29. 2008
    ....
  20. ncbi Selective presynaptic degeneration in the synaptopathy associated with ME7-induced hippocampal pathology
    Bryony C Gray
    School of Biological Sciences, University of Southampton, Bassett Crescent East, Southampton, Hants, UK
    Neurobiol Dis 35:63-74. 2009
    ..This synaptic pathology or "synaptopathy" may represent the earliest neuronal dysfunction in this and other protein misfolding induced neurodegenerative diseases...
  21. ncbi Differential induction of interleukin-1beta and tumour necrosis factor-alpha may account for specific patterns of leukocyte recruitment in the brain
    Donatienne Blond
    CNS Inflammation Group, School of Biological Sciences, University of Southampton, Biomedical Sciences Building, Southampton SO16 7PX, UK
    Brain Res 958:89-99. 2002
    ....
  22. ncbi Synaptic changes characterize early behavioural signs in the ME7 model of murine prion disease
    C Cunningham
    CNS Inflammation Group, Southampton Neuroscience Group, School of Biological Sciences, University of Southampton, Southampton SO16 7PX, UK
    Eur J Neurosci 17:2147-55. 2003
    ..We have demonstrated a neuropathological correlate of an early behavioural deficit in prion disease and suggest that this should allow insights into the first steps of the neuropathogenesis of prion diseases...
  23. ncbi Proinflammatory cytokines, sickness behavior, and Alzheimer disease
    C Holmes
    University of Southampton, Memory Assessment and Research Centre, Botley Rd, Southampton, UK, SO30 3JB
    Neurology 77:212-8. 2011
    ....
  24. ncbi Systemic infection and inflammation in acute CNS injury and chronic neurodegeneration: underlying mechanisms
    J L Teeling
    CNS Inflammation Group, School of Biological Sciences, University of Southampton, Biomedical Sciences Building, Bassett Crescent East, Southampton SO16 7PX, UK
    Neuroscience 158:1062-73. 2009
    ..In this review we discuss the underlying mechanisms responsible for sickness behavior induced by systemic inflammation in the healthy brain and how they might be different in individuals with CNS pathology...
  25. ncbi The systemic and local acute phase response following acute brain injury
    David C Wilcockson
    CNS Inflammation Group, School of Biological Sciences, University of Southampton, Southampton, Hampshire, UK
    J Cereb Blood Flow Metab 22:318-26. 2002
    ..These results suggest that the local APR may play a role as an antiinflammatory mechanism. These findings indicate a potentially pivotal role for peripheral and local APP production on outcome after brain injury...
  26. ncbi Cytokine-induced enhancement of autoimmune inflammation in the brain and spinal cord: implications for multiple sclerosis
    D Sun
    Pathology and Clinical Neurosciences (Neuropathology, University of Southampton, Southampton, UK
    Neuropathol Appl Neurobiol 30:374-84. 2004
    ..Conclusion: local changes in the release of pro-inflammatory cytokines within the brain in EAE results in the widespread enhancement of autoimmune inflammation within the brain and cord, and exacerbation of clinical symptoms...
  27. ncbi Differential regulation of type I and type II interleukin-1 receptors in focal brain inflammation
    Fabian Docagne
    Molecular Neuropathology Laboratory, School of Biological Sciences, University of Southampton, UK
    Eur J Neurosci 21:1205-14. 2005
    ..The lesion-specific expression of IL-1 receptors suggests that the receptors are differentially regulated in a manner not directly related to the endogenous level of IL-1 in the CNS...
  28. ncbi Reduction of excitotoxicity and associated leukocyte recruitment by a broad-spectrum matrix metalloproteinase inhibitor
    Sandra J Campbell
    Molecular Neuropathology Laboratory, School of Biological Sciences, University of Southampton, Biomedical Sciences Building, Southampton SO16 7PX, UK
    J Neurochem 89:1378-86. 2004
    ..These studies suggest that MMP inhibitors have therapeutic potential for use in stroke, and support the increasing evidence that microglial activation may contribute to neuronal cell death...
  29. ncbi Increased expression of glial fibrillary acidic protein fragments and mu-calpain activation within the hippocampus of prion-infected mice
    B C Gray
    Neurosciences Group, School of Biological Sciences, University of Southampton, Southampton SO16 7PX, UK
    Biochem Soc Trans 34:51-4. 2006
    ..It may therefore contribute to the reactive gliosis that is characteristic of prion diseases...
  30. ncbi Recruitment of neutrophils across the blood-brain barrier: the role of E- and P-selectins
    M Bernardes-Silva
    CNS Inflammation Group, School of Biological Sciences, Biomedical Sciences Building, University of Southampton, UK
    J Cereb Blood Flow Metab 21:1115-24. 2001
    ..Surprisingly, E-selectin blockade had no effect on neutrophil recruitment to the brain parenchyma. Thus, P-selectin appears to play a pivotal role in mediating neutrophil recruitment to the brain parenchyma during acute inflammation...
  31. ncbi Nramp1 modulates iron homoeostasis in vivo and in vitro: evidence for a role in cellular iron release involving de-acidification of intracellular vesicles
    T E Biggs
    Biochemistry and Molecular Biology, School of Biological Sciences, Southampton, GB, UK
    Eur J Immunol 31:2060-70. 2001
    ..This study demonstrates that Nramp1 regulates macrophage iron handling, and probably facilitates iron release from macrophages undergoing erythrophagocytosis in vivo...
  32. ncbi Solutes, but not cells, drain from the brain parenchyma along basement membranes of capillaries and arteries: significance for cerebral amyloid angiopathy and neuroimmunology
    R O Carare
    Clinical Neurosciences, University of Southampton, UK
    Neuropathol Appl Neurobiol 34:131-44. 2008
    ..This atypical pattern of drainage may contribute to partial immune privilege of the brain and play a role in neuroimmunological diseases such as multiple sclerosis...
  33. ncbi [The evidence for primary axonal loss in multiple sclerosis]
    D C Anthony
    Grupo para las inflamaciones del SNC, Escuela de Ciencias Biologicas, University of Southampton, Inglaterra
    Rev Neurol 30:1203-8. 2000
    ....
  34. ncbi Immune-to-brain signalling: the role of cerebral CD163-positive macrophages
    Ian Galea
    CNS Inflammation Group, School of Biological Sciences, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, UK
    Neurosci Lett 448:41-6. 2008
    ..Cerebral endothelial cells outnumber CD163-positive macrophages and are arguably better situated to signal circulating inflammatory stimuli to the brain...
  35. ncbi Transforming growth factor-beta 1-mediated neuroprotection against excitotoxic injury in vivo
    Delphine Boche
    CNS Inflammation Group, Southampton Neuroscience Group, School of Biological Sciences, University of Southampton, Southampton, Hampshire, UK
    J Cereb Blood Flow Metab 23:1174-82. 2003
    ..We have demonstrated in vivo that the cerebral tolerance phenomenon induced by LPS pretreatment is mediated by TGF-beta 1 cytokine...
  36. ncbi Low protein diet fed exclusively during mouse oocyte maturation leads to behavioural and cardiovascular abnormalities in offspring
    Adam J Watkins
    School of Biological Sciences, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, UK
    J Physiol 586:2231-44. 2008
    ..Similar and distinct postnatal outcomes were observed here compared with maternal LPD treatment during post-fertilization preimplantation development which may reflect the relative contribution of the paternal genome...
  37. ncbi Reactive hypertrophy of synaptic varicosities within the hippocampus of prion-infected mice
    Zuzana Siskova
    CNS Inflammation Group, Basset Crescent East, School of Biological Sciences, University of Southampton, Southampton SO16 7PX, UK
    Biochem Soc Trans 38:471-5. 2010
    ....
  38. ncbi Altered chemokine expression in the spinal cord and brain contributes to differential interleukin-1beta-induced neutrophil recruitment
    Sandra J Campbell
    Molecular Neuropathology Laboratory and CNS Inflammation Group, School of Biological Sciences, University of Southampton, Southampton, UK
    J Neurochem 83:432-41. 2002
    ..No expression of CINC-2beta mRNA was detected. Thus differential chemokine induction may contribute to variations in neutrophil recruitment in during development and between the different CNS compartments...
  39. ncbi TGFbeta1 regulates the inflammatory response during chronic neurodegeneration
    Delphine Boche
    CNS Inflammation Group, Southampton Neurosciences Group, School of Biological Sciences, University of Southampton, Southampton, SO16 7PX Hampshire, UK
    Neurobiol Dis 22:638-50. 2006
    ..These data suggest that TGFbeta1 plays a critical role in the downregulation of microglial responses minimizing brain inflammation and thus avoiding exacerbation of brain damage...
  40. ncbi CINC-1 is an acute-phase protein induced by focal brain injury causing leukocyte mobilization and liver injury
    Sandra J Campbell
    Molecular Neuropathology Laboratory, School of Biological Sciences, University of Southampton, Biomedical Sciences Building, Southampton S016 7PX, UK
    FASEB J 17:1168-70. 2003
    ..Hepatic CINC-1 synthesis following injury presents a novel focus for treatment of inflammation...
  41. ncbi Central and systemic endotoxin challenges exacerbate the local inflammatory response and increase neuronal death during chronic neurodegeneration
    Colm Cunningham
    CNS Inflammation Group, School of Biological Sciences, Southampton, Hampshire SO16 7PX, United Kingdom
    J Neurosci 25:9275-84. 2005
    ..The finding that a single acute systemic inflammatory event can induce neuronal death in the CNS has implications for therapy in neurodegenerative diseases...
  42. ncbi What is immune privilege (not)?
    Ian Galea
    CNS Inflammation Group, School of Biological Sciences, University of Southampton, SO16 7PX, UK
    Trends Immunol 28:12-8. 2007
    ..It is now increasingly recognized how immune privilege is maintained actively as a result of the immunoregulatory characteristics of the CNS-resident cells and their microenvironment...
  43. ncbi Unaltered SNARE complex formation in an in vivo model of prion disease
    Ayodeji A Asuni
    School of Biological Sciences, University of Southampton, Bassett Crescent East, Southampton, SO16 7PX, UK
    Brain Res 1233:1-7. 2008
    ..Thus the accumulation of PrP(Sc) although deleterious to synaptic function in vivo, does not exert its synaptic effects by disrupting the formation of SNARE complexes that are core to transmitter release...
  44. ncbi Blood-derived dendritic cells in an acute brain injury
    Tracey A Newman
    CNS Inflammation Group, University of Southampton, UK
    J Neuroimmunol 166:167-72. 2005
    ..We conclude that DC are recruited to an excitotoxic lesion from a blood-derived cell population. This may have implications for neuropathologies involving DC recruitment...
  45. ncbi Association between dementia and infectious disease: evidence from a case-control study
    Nicholas Dunn
    University of Southampton, UK
    Alzheimer Dis Assoc Disord 19:91-4. 2005
    ..Smoking and diabetes mellitus are associated with onset of dementia in the elderly. The evidence from this study may represent cause and effect, since there is a credible biologic explanation...
  46. ncbi Microglia in neurodegenerative disease
    V Hugh Perry
    School of Biological Sciences, University of Southampton, Building 62, Boldrewood Campus, Southampton SO16 7PX, UK
    Nat Rev Neurol 6:193-201. 2010
    ..The fact that diseases with a chronic systemic inflammatory component are risk factors for Alzheimer disease implies that crosstalk occurs between systemic inflammation and microglia in the CNS...
  47. ncbi Mannose receptor expression specifically reveals perivascular macrophages in normal, injured, and diseased mouse brain
    Ian Galea
    CNS Inflammation Group, School of Biological Sciences, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, UK
    Glia 49:375-84. 2005
    ....
  48. ncbi Comparison of inflammatory and acute-phase responses in the brain and peripheral organs of the ME7 model of prion disease
    Colm Cunningham
    CNS Inflammation Group, School of Biological Sciences, Bassett Crescent East, Southampton, Hampshire SO16 7PX, United Kingdom
    J Virol 79:5174-84. 2005
    ..We also propose that serum cytokine and APP measurements are not useful during preclinical disease. Possible consequences of the clear chronic elevation of APPs in the CNS are discussed...
  49. ncbi An antigen-specific pathway for CD8 T cells across the blood-brain barrier
    Ian Galea
    CNS Inflammation Group, School of Biological Sciences, University of Southampton, Southampton, UK
    J Exp Med 204:2023-30. 2007
    ..This has implications for a variety of diseases in which antigen-specific CD8 T cell traffic into the brain is a beneficial or deleterious feature...
  50. ncbi Transforming growth factor beta1, the dominant cytokine in murine prion disease: influence on inflammatory cytokine synthesis and alteration of vascular extracellular matrix
    C Cunningham
    CNS Inflammation Group, School of Biological Sciences, University of Southampton SO16 7PX, UK
    Neuropathol Appl Neurobiol 28:107-19. 2002
    ..These findings suggest that TGF-beta1 may play a central role in maintenance of an atypical microglial phenotype and may also be involved in vascular and extracellular matrix changes...
  51. ncbi The cellular distribution of the Wld s chimeric protein and its constituent proteins in the CNS
    C Fang
    CNS Inflammation Group, Southampton Neuroscience Group, School of Biological Sciences, Biomedical Sciences Building, University of Southampton, Southampton SO16 7PX, UK
    Neuroscience 135:1107-18. 2005
    ..The increased Nmnat-1 activity in the nucleus of Wld s mice compared with wild-type mice seems to be a significant factor in the axon protection. It is not known whether the expression of the Nmnat-1 in the axon is significant...
  52. ncbi Self-destruct programs in the processes of developing neurons
    David Shepherd
    School of Biological Sciences, University of Southampton, Southampton SO16 7PX, United Kingdom
    Curr Top Dev Biol 65:149-67. 2005
  53. ncbi Characterization of the murine Nramp1 promoter: requirements for transactivation by Miz-1
    Holly Bowen
    Division of Biochemistry and Molecular Biology, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, United Kingdom
    J Biol Chem 278:36017-26. 2003
    ....
  54. ncbi Change in tau phosphorylation associated with neurodegeneration in the ME7 model of prion disease
    Ayodeji A Asuni
    CNS Inflammation Group, University of Southampton, Southampton SO16 7PX, UK
    Biochem Soc Trans 38:545-51. 2010
    ..These data suggest that the changes in tau phosphorylation recorded here and observed by others relate to end-stage prion pathology when early dysfunctions have progressed to overt neuronal loss...
  55. ncbi Review: activation patterns of microglia and their identification in the human brain
    D Boche
    Clinical Neurosciences, Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, UK
    Neuropathol Appl Neurobiol 39:3-18. 2013
    ....
  56. ncbi Systemic infection, interleukin 1beta, and cognitive decline in Alzheimer's disease
    C Holmes
    School of Medicine and Biological Sciences, University of Southampton, Southampton, UK
    J Neurol Neurosurg Psychiatry 74:788-9. 2003
    ..Further research is needed to determine whether recurrent systemic infections drive cognitive decline in Alzheimer's disease subjects through a cytokine mediated pathway...
  57. ncbi Mechanisms to explain the reverse perivascular transport of solutes out of the brain
    D Schley
    Department of Medical Physics and Bioengineering, Southampton University Hospitals NHS Trust, Southampton General Hospital, Southampton, Hampshire SO16 6YD, UK
    J Theor Biol 238:962-74. 2006
    ..These factors may play a role in the pathogenesis of cerebral amyloid angiopathy and in the accumulation of Abeta in the brain in Alzheimer's disease...
  58. ncbi Comparison of matrix metalloproteinase expression during Wallerian degeneration in the central and peripheral nervous systems
    P M Hughes
    Nurin Ltd, CNS Inflammation Group, Biomedical Sciences Building, University of Southampton, Southampton SO16 7PX, UK
    Neuroscience 113:273-87. 2002
    ....
  59. ncbi Selective effects of upper respiratory tract infection on cognition, mood and emotion processing: a prospective study
    Romola S Bucks
    University of Southampton, UK
    Brain Behav Immun 22:399-407. 2008
    ..URTIs also affect mood. Future studies need to examine the role of inflammatory molecules and the brain regions implicated in mediating these findings...
  60. ncbi Influence of the course of brain inflammation on the endogenous IL-1beta/IL-1Ra balance in the model of brain delayed-type hypersensitivity response to bacillus Calmette-Guérin in Lewis rats
    Karine Palin
    INRA UMR 1244, Université V Segalen Bordeaux 2, FRE CNRS Institut François Magendie, rue Camille Saint Saens, 33077 Bordeaux Cedex, France
    J Neuroimmunol 149:22-30. 2004
    ..Besides showing that the course of inflammation alters the brain IL-1beta/IL-1Ra ratio, these findings point to the importance of monitoring plasma IL-1beta/IL-1Ra ratio to predict the course of brain inflammation...
  61. ncbi Reversible demyelination, blood-brain barrier breakdown, and pronounced neutrophil recruitment induced by chronic IL-1 expression in the brain
    Carina C Ferrari
    Leloir Institute, Universiity of Buenos Aires, Buenos Aires, Argentina
    Am J Pathol 165:1827-37. 2004
    ....
  62. ncbi Inhibition of alpha-glucosidases I and II increases the cell surface expression of functional class A macrophage scavenger receptor (SR-A) by extending its half-life
    Gang Tian
    Department of Cardiology, First Hospital, Xi an Jiaotong University, Jiankang Road, Xi an 710061, China
    J Biol Chem 279:39303-9. 2004
    ..SR-A interacts with calnexin and when the association is prevented changes in the recycling kinetics and rate of turnover of the receptor result, leading to enhanced cell surface expression...
  63. ncbi Central nervous system inflammation is a hallmark of pathogenesis in mouse models of GM1 and GM2 gangliosidosis
    M Jeyakumar
    Glycobiology Institute, Department of Biochemistry, University of Oxford, Oxford, UK
    Brain 126:974-87. 2003
    ..These data suggest that inflammation may play an important role in the pathogenesis of the gangliosidoses...
  64. ncbi MRI and MRS alterations in the preclinical phase of murine prion disease: association with neuropathological and behavioural changes
    Kerry A Broom
    Experimental Neuroimaging Group, Department of Physiology, Anatomy and Genetics, University of Oxford, Sherrington Building, Parks Rd, Oxford, OX1 3PT, UK
    Neurobiol Dis 26:707-17. 2007
    ..These changes in MRI and MRS signals, which precede overt clinical signs of disease, could provide insights into the pathogenesis of this disease and may enable early detection of pathology...
  65. ncbi Central nervous system injury triggers hepatic CC and CXC chemokine expression that is associated with leukocyte mobilization and recruitment to both the central nervous system and the liver
    Sandra J Campbell
    Department of Pharmacology, University of Oxford, Oxfordshire OX1 3QT, United Kingdom
    Am J Pathol 166:1487-97. 2005
    ..Thus, combined production of CC and CXC hepatic chemokines appears to amplify the central nervous system response to injury...
  66. ncbi TNF-alpha reduces cerebral blood volume and disrupts tissue homeostasis via an endothelin- and TNFR2-dependent pathway
    Nicola R Sibson
    MRC Biochemical and Clinical Magnetic Resonance Unit, Department of Biochemistry, University of Oxford, UK
    Brain 125:2446-59. 2002
    ....
  67. ncbi What is the blood-brain barrier (not)?
    Ingo Bechmann
    Dr Senckenbergische Anatomie, Institute of Clinical Neuroanatomy, Johann Wolfgang Goethe University, 60 590 Frankfurt, Germany
    Trends Immunol 28:5-11. 2007
    ..We propose that the second step frequently involves perivascular antigen-recognition and the induction of ectoenzymes, for example matrix metalloproteinases (MMPs)...
  68. ncbi Summary of the 12th Nikolas Symposium dendritic cell differentiation: signals, signaling and functional consequences as clues to possible therapy
    Kim E Nichols
    Division of Pediatric Oncology, Children's of Hospital Philadelphia, Philadelphia, Pensilvania 19104, USA
    J Pediatr Hematol Oncol 25:193-7. 2003
  69. ncbi Axon pathology in neurological disease: a neglected therapeutic target
    Michael P Coleman
    Center for Molecular Medicine ZMMK and Institute for Genetics, University of Cologne, Zuelpicher Strasse 47, Germany
    Trends Neurosci 25:532-7. 2002
    ..Understanding how these diverse insults might initiate an axon-degeneration process could lead to new therapeutic interventions...
  70. ncbi Retinoic acid-inducible gene-I mediates late phase induction of TNF-alpha by lipopolysaccharide
    Jing Wang
    National Laboratory of Protein Engineering and Plant Genetic Engineering, College of Life Sciences, Peking University, Beijing, China
    J Immunol 180:8011-9. 2008
    ..Thus, RIG-I plays a key role in the expression of TNF-alpha in macrophages in response to LPS stimulation, mainly for the late phase LPS-induced expression of TNF-alpha...
  71. ncbi Monocyte chemoattractant protein-1 deficiency is protective in a murine stroke model
    Paula M Hughes
    Nervous System Research, Core Technology Area, Novartis Pharma AG, Basel, Switzerland
    J Cereb Blood Flow Metab 22:308-17. 2002
    ..The results of this study indicate that inhibition of MCP-1 signaling could be a new acute treatment approach to limit infarct size after stroke...
  72. ncbi c-Myc represses and Miz-1 activates the murine natural resistance-associated protein 1 promoter
    Holly Bowen
    Biochemistry and Molecular Biology, University of Southampton, Bassett Crescent East, United Kingdom
    J Biol Chem 277:34997-5006. 2002
    ..The results provide further support for a divalent cation antiporter function for Nramp1...
  73. ncbi Hippocampal scrapie infection impairs operant DRL performance in mice
    Robert M J Deacon
    Department of Experimental Psychology, University of Oxford, South Parks Road, Oxford OX1 3UD, UK
    Behav Brain Res 157:99-105. 2005
    ....
  74. ncbi An inducible mouse model of late onset Tay-Sachs disease
    Mylvaganam Jeyakumar
    Glycobiology Institute, Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, United Kingdom
    Neurobiol Dis 10:201-10. 2002
    ..Repeat breeding of a large cohort of female Tay-Sachs mice confirmed that pregnancy induces late onset Tay-Sachs disease. Onset of symptoms correlated with reduced up-regulation of hexosaminidase B, a component of the bypass pathway...