Seth Love

Summary

Affiliation: University of Bristol
Country: UK

Publications

  1. pmc Neuropathological investigation of dementia: a guide for neurologists
    S Love
    Department of Neuropathology, University of Bristol Institute of Clinical Neurosciences, Clinical Science at North Bristol, Frenchay Hospital, Bristol, UK
    J Neurol Neurosurg Psychiatry 76:v8-14. 2005
  2. pmc Resistant to amyloid-β or just waiting for disease to happen?
    Seth Love
    Dementia Research Group, Institute of Clinical Neurosciences School of Clinical Sciences, University of Bristol, Frenchay Hospital, Bristol, BS16 1LE, UK
    Alzheimers Res Ther 4:19. 2012
  3. doi Autopsy approach to stroke
    Seth Love
    Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol, UK
    Histopathology 58:333-51. 2011
  4. ncbi APOE and cerebral amyloid angiopathy in the elderly
    Seth Love
    Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK
    Neuroreport 14:1535-6. 2003
  5. ncbi Neuronal expression of cell cycle-related proteins after brain ischaemia in man
    Seth Love
    Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK
    Neurosci Lett 353:29-32. 2003
  6. ncbi Trigeminal neuralgia: pathology and pathogenesis
    S Love
    Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK
    Brain 124:2347-60. 2001
  7. ncbi Insights into the pathogenesis and pathogenicity of cerebral amyloid angiopathy
    Seth Love
    Dementia Research Group, University of Bristol Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK
    Front Biosci (Landmark Ed) 14:4778-92. 2009
  8. ncbi Chronic granulomatous herpes simplex encephalitis in children
    Seth Love
    Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol, United Kingdom
    J Neuropathol Exp Neurol 63:1173-81. 2004
  9. ncbi Premorbid effects of APOE on synaptic proteins in human temporal neocortex
    Seth Love
    Department of Neuropathology, University of Bristol Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK
    Neurobiol Aging 27:797-803. 2006
  10. ncbi Ruptured vertebrobasilar aneurysm associated with giant cell arteritis in a young boy
    Seth Love
    Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK
    Clin Neurol Neurosurg 110:92-6. 2008

Detail Information

Publications95

  1. pmc Neuropathological investigation of dementia: a guide for neurologists
    S Love
    Department of Neuropathology, University of Bristol Institute of Clinical Neurosciences, Clinical Science at North Bristol, Frenchay Hospital, Bristol, UK
    J Neurol Neurosurg Psychiatry 76:v8-14. 2005
  2. pmc Resistant to amyloid-β or just waiting for disease to happen?
    Seth Love
    Dementia Research Group, Institute of Clinical Neurosciences School of Clinical Sciences, University of Bristol, Frenchay Hospital, Bristol, BS16 1LE, UK
    Alzheimers Res Ther 4:19. 2012
    ..The study emphasizes the continuing importance of careful human clinical and post-mortem studies in elucidating the pathogenesis of this disease...
  3. doi Autopsy approach to stroke
    Seth Love
    Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol, UK
    Histopathology 58:333-51. 2011
    ....
  4. ncbi APOE and cerebral amyloid angiopathy in the elderly
    Seth Love
    Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK
    Neuroreport 14:1535-6. 2003
    ..028). Possession of epsilon4 does not by itself confer an increased risk of CAA but may be associated with reduced longevity even in the absence of AD or cerebral haemorrhage...
  5. ncbi Neuronal expression of cell cycle-related proteins after brain ischaemia in man
    Seth Love
    Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK
    Neurosci Lett 353:29-32. 2003
    ..Present findings indicate that brain ischaemia induces the entry of some neurons from G0 into the G1 phase of the cell cycle, and suggest a potential therapeutic role for CDK inhibitors in ischaemic stroke...
  6. ncbi Trigeminal neuralgia: pathology and pathogenesis
    S Love
    Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK
    Brain 124:2347-60. 2001
    ..Clinical observations and electrophysiological studies support the concept that demyelination and ephaptic spread of excitation underlie most, if not all, of these conditions...
  7. ncbi Insights into the pathogenesis and pathogenicity of cerebral amyloid angiopathy
    Seth Love
    Dementia Research Group, University of Bristol Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK
    Front Biosci (Landmark Ed) 14:4778-92. 2009
    ..The balance between parenchymal and cerebrovascular degradation of Abeta, and regulation of perivascular extracellular matrix production, are likely to be key determinants of Abeta distribution and pathogenicity within the brain...
  8. ncbi Chronic granulomatous herpes simplex encephalitis in children
    Seth Love
    Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol, United Kingdom
    J Neuropathol Exp Neurol 63:1173-81. 2004
    ..This pattern of disease may be an under-recognized complication of herpes simplex infection during the first few years of life...
  9. ncbi Premorbid effects of APOE on synaptic proteins in human temporal neocortex
    Seth Love
    Department of Neuropathology, University of Bristol Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK
    Neurobiol Aging 27:797-803. 2006
    ..01). APOE influences the concentration of synaptic proteins in normal superior temporal cortex and may thereby affect the response to injury, and the risk and outcome of a range of neurologic diseases...
  10. ncbi Ruptured vertebrobasilar aneurysm associated with giant cell arteritis in a young boy
    Seth Love
    Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK
    Clin Neurol Neurosurg 110:92-6. 2008
    ..The findings highlight the need for detailed examination in such cases, to elucidate the pathogenesis and pathology of cerebrovascular aneurysms in this age group...
  11. pmc Demyelinating diseases
    S Love
    Department of Neuropathology, University of Bristol Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK
    J Clin Pathol 59:1151-9. 2006
    ..Freezing of a small amount of fresh tissue allows for later virological studies, and electron microscopy is occasionally helpful for demonstration of viral particles...
  12. ncbi Apoptosis and brain ischaemia
    Seth Love
    Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, BS16 1LE, Bristol, UK
    Prog Neuropsychopharmacol Biol Psychiatry 27:267-82. 2003
    ....
  13. ncbi Expression of P-selectin and intercellular adhesion molecule-1 in human brain after focal infarction or cardiac arrest
    S Love
    Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol, UK
    Neuropathol Appl Neurobiol 27:465-73. 2001
    ..The finding that P-selectin and ICAM-1 are upregulated within focally infarcted brain tissue supports the concept that blocking neutrophil adhesion may be of benefit in treating atherothrombotic strokes in man...
  14. ncbi Methods for detection of haematogenous dissemination of brain tissue after stunning of cattle with captive bolt guns
    S Love
    Department of Neuropathology, Frenchay Hospital, BS161LE, Bristol, UK
    J Neurosci Methods 99:53-8. 2000
    ..The described methods should allow an assessment of the risk of neuroembolism associated with different types of CBG and may also be useful in other contexts...
  15. ncbi Neuronal death in brain infarcts in man
    S Love
    Departments of Neuropathology, Care of the Elderly, Frenchay Hospital, Bristol, UK
    Neuropathol Appl Neurobiol 26:55-66. 2000
    ....
  16. ncbi Oxidative stress in brain ischemia
    S Love
    Department of Neuropathology, Frenchay Hospital, Bristol, UK
    Brain Pathol 9:119-31. 1999
    ..The findings in recent animal studies are likely to lead to a range of further pharmacological strategies to limit brain injury in stroke patients...
  17. ncbi Trigeminal neuralgia due to multiple sclerosis: ultrastructural findings in trigeminal rhizotomy specimens
    S Love
    Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK
    Neuropathol Appl Neurobiol 27:238-44. 2001
    ..The demyelination and associated juxtaposition of axons may therefore account for key aspects of the pathogenesis of trigeminal neuralgia...
  18. ncbi Increased poly(ADP-ribosyl)ation of nuclear proteins in Alzheimer's disease
    S Love
    Department of Neuropathology, Frenchay Hospital, Bristol, UK
    Brain 122:247-53. 1999
    ..Our findings indicate that there is enhanced PARP activity in Alzheimer's disease and suggest that pharmacological interventions aimed at inhibiting PARP may have a role in slowing the progression of the disease...
  19. ncbi TNFR-associated factor-2 (TRAF-2) in Alzheimer's disease
    Doris Culpan
    Dementia Research Group, Institute of Clinical Neurosciences, Department of Clinical Sciences at North Bristol, University of Bristol, John James Buildings, Frenchay Hospital, Bristol, United Kingdom
    Neurobiol Aging 30:1052-60. 2009
    ..The 3' UTR SNP (rs7852970) GG allele was significantly protective against AD (p=0.030). Our findings suggest that the TRAF-2 pathway is involved AD. The mechanisms are currently unclear and need further examination...
  20. doi Oxidative balance in Alzheimer's disease: relationship to APOE, Braak tangle stage, and the concentrations of soluble and insoluble amyloid-β
    Hannah Tayler
    Dementia Research Group, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol, UK
    J Alzheimers Dis 22:1363-73. 2010
    ..Increased β-secretase activity associated with oxidative stress is likely to contribute to the accumulation of Aβ and this, in turn, to induce antioxidant capacity...
  21. doi Fatty acid composition of frontal, temporal and parietal neocortex in the normal human brain and in Alzheimer's disease
    Thomas Fraser
    Dementia Research Group, Institute of Clinical Neurosciences, University of Bristol, Frenchay Hospital, Bristol, BS16 1LE, UK
    Neurochem Res 35:503-13. 2010
    ..Fatty acid composition was not related to APOE genotype, age, gender or post-mortem delay. Further research is needed to distinguish between alterations that are secondary to AD and those that contribute to the disease process...
  22. doi Oligomeric Abeta in Alzheimer's disease: relationship to plaque and tangle pathology, APOE genotype and cerebral amyloid angiopathy
    Zoë van Helmond
    Dementia Research Group, Institute of Clinical Neurosciences, Clinical Science at North Bristol, University of Bristol, Bristol, UK
    Brain Pathol 20:468-80. 2010
    ....
  23. doi Elevated matrix metalloproteinase-9 and degradation of perineuronal nets in cerebrocortical multiple sclerosis plaques
    Elizabeth Gray
    MS Laboratories, Burden Centre, University of Bristol Institute of Clinical Neurosciences, Frenchay Hospital, Bristol, UK
    J Neuropathol Exp Neurol 67:888-99. 2008
    ..Matrix metalloproteinase-mediated degradation of PNs in cortical plaques may, therefore, contribute to neuronal dysfunction and degeneration in MS patients...
  24. doi Endothelin-1 is elevated in Alzheimer's disease and upregulated by amyloid-β
    Jennifer C Palmer
    Dementia ResearchGroup, School of Clinical Sciences, University of Bristol, Frenchay Hospital, Bristol, UK
    J Alzheimers Dis 29:853-61. 2012
    ..024). These findings provide evidence of overactivity of the endothelin system in AD, further supporting the suggestion that endothelin receptor antagonists may be of value for the treatment of this disease...
  25. ncbi Elevated activity and microglial expression of myeloperoxidase in demyelinated cerebral cortex in multiple sclerosis
    Elizabeth Gray
    Glial Cell Biology Laboratories, University of Bristol Institute of Clinical Neuroscience, Frenchay Hospital, Bristol, UK
    Brain Pathol 18:86-95. 2008
    ....
  26. doi Loss of Perineuronal Net in ME7 Prion Disease
    Sarah L Franklin
    MRC Centre for Synaptic Plasticity, University of Bristol, Bristol, United Kingdom
    J Neuropathol Exp Neurol 67:189-99. 2008
    ..Our findings suggest that the substrate of the earliest synaptic and behavioral abnormalities in murine prion disease may be inflammatory microglia-mediated degradation of the PN...
  27. doi Higher soluble amyloid beta concentration in frontal cortex of young adults than in normal elderly or Alzheimer's disease
    Zoë van Helmond
    Dementia Research Group, Institute of Clinical Neurosciences, Clinical Science at North Bristol, University of Bristol, UK
    Brain Pathol 20:787-93. 2010
    ....
  28. pmc Pathophysiology of white matter perfusion in Alzheimer's disease and vascular dementia
    Rachel Barker
    1 Dementia Research Group, Institute of Clinical Neurosciences, School of Clinical Sciences, University of Bristol, Bristol, UK
    Brain 137:1524-32. 2014
    ....
  29. doi Accumulation of cortical hyperphosphorylated neurofilaments as a marker of neurodegeneration in multiple sclerosis
    Elizabeth Gray
    MS Labs, Burden Centre, University of Bristol Institute of Clinical Neurosciences, Frenchay Hospital, UK
    Mult Scler 19:153-61. 2013
    ..Perikaryal accumulation of abnormally phosphorylated neurofilament proteins has been reported in some neurodegenerative diseases...
  30. pmc Endothelin-converting enzyme-2 is increased in Alzheimer's disease and up-regulated by Abeta
    Jennifer C Palmer
    Dementia Research Group, Frenchay Hospital, Bristol, United Kingdom
    Am J Pathol 175:262-70. 2009
    ..Our findings suggest that endothelin-1 receptor antagonists, already licensed for treating other diseases, could be of benefit in AD therapies...
  31. doi Cholinesterase inhibitors may increase phosphorylated tau in Alzheimer's disease
    Katy A Chalmers
    Dementia Research Group, Department of Clinical Science at North Bristol, University of Bristol, Bristol, UK
    J Neurol 256:717-20. 2009
    ..004). Abeta accumulation was reduced but not significantly. These data raise the possibility that increased tau phosphorylation may influence long-term clinical responsiveness to ChEIs...
  32. doi Changes with age in the activities of beta-secretase and the Abeta-degrading enzymes neprilysin, insulin-degrading enzyme and angiotensin-converting enzyme
    J Scott Miners
    Dementia Research Group, Institute of Clinical Neurosciences, Clinical Science at North Bristol, University of Bristol, Bristol, UK
    Brain Pathol 20:794-802. 2010
    ..Further research is needed to establish whether these changes in enzyme activity and Abeta levels are causally related and if so how...
  33. doi Kallikrein-related peptidase 6 in Alzheimer's disease and vascular dementia
    Emma L Ashby
    Dementia Research Group, Institute of Clinical Neurosciences, Clinical Science at North Bristol, University of Bristol, UK
    Brain Res 1363:1-10. 2010
    ..In VaD, KLK6 protein level was significantly increased in the frontal cortex. Our findings suggest that an altered KLK6 expression may contribute to vascular abnormalities in AD and VaD...
  34. ncbi Neprilysin and insulin-degrading enzyme levels are increased in Alzheimer disease in relation to disease severity
    James Scott Miners
    Dementia Research Group, Clinical Science at North Bristol, University of Bristol, Frenchay Hospital, Frenchay, Bristol, United Kingdom
    J Neuropathol Exp Neurol 68:902-14. 2009
    ..Our findings suggest that reduction in NEP and IDE activity is not the primary cause of beta-amyloid accumulation in AD, but rather a late-stage phenomenon secondary to neurodegeneration...
  35. doi Aβ-degrading enzymes: potential for treatment of Alzheimer disease
    James Scott Miners
    Dementia Research Group, Institute of Clinical Neurosciences, Clinical Science at North Bristol, University of Bristol, Frenchay Hospital, UK
    J Neuropathol Exp Neurol 70:944-59. 2011
    ..In the longer term, genetic approaches to increasing the intracerebral expression of NEP or other Aβ-degrading enzymes may offer advantages...
  36. ncbi Damage to nuclear DNA in Lewy body disease
    S Love
    Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK
    Neuroreport 12:2725-9. 2001
    ..Caspase-3 activity was largely restricted to microglia but was detected in an occasional nigral neuron. Nuclear DNA damage occurs in vivo in LBD but only rarely indicates neuronal apoptosis...
  37. pmc Assessing white matter ischemic damage in dementia patients by measurement of myelin proteins
    Rachel Barker
    Dementia Research Group, Institute of Clinical Neurosciences, School of Clinical Sciences, University of Bristol, Bristol, UK
    J Cereb Blood Flow Metab 33:1050-7. 2013
    ..MAG concentration and the MAG/PLP ratio are useful post-mortem measures of ante-mortem white matter ischemia. ..
  38. doi Assessment of activation of the plasma kallikrein-kinin system in frontal and temporal cortex in Alzheimer's disease and vascular dementia
    Emma L Ashby
    Dementia Research Group, Institute of Clinical Neurosciences, School of Clinical Sciences, University of Bristol, Bristol, UK
    Neurobiol Aging 33:1345-55. 2012
    ..PK activity was significantly increased in the frontal and temporal cortex in AD. Increased PK activity in AD is likely to contribute to increased BK release and may thereby influence cerebral blood flow and vascular permeability...
  39. ncbi Convection-enhanced delivery of neprilysin: a novel amyloid-β-degrading therapeutic strategy
    Neil U Barua
    Functional Neurosurgery Research Group, University of Bristol, Bristol, UK
    J Alzheimers Dis 32:43-56. 2012
    ..CED of NEP has therapeutic potential as a dynamically controllable Aβ(40)-degrading therapeutic strategy for AD. Further studies are required to determine the longer term effects on Aβ (including Aβ(42)) and on cognitive function...
  40. ncbi Neither sequence variation in the IL-10 gene promoter nor presence of IL-10 protein in the cerebral cortex is associated with Alzheimer's disease
    Doris Culpan
    Dementia Research Group, Institute of Clinical Neurosciences, Department of Clinical Sciences at North Bristol, University of Bristol, John James Buildings, Frenchay Hospital, Frenchay, Bristol, BS16 1LE, United Kingdom
    Neurosci Lett 408:141-5. 2006
    ..Levels of IL-10 protein and gene expression examined also did not appear to be related to AD. Despite this being a relatively small sample, these data suggest that IL-10 does not play a major role in the development of AD...
  41. doi Elevated myeloperoxidase activity in white matter in multiple sclerosis
    Elizabeth Gray
    MS Laboratories, Burden Centre, University of Bristol Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1JB, United Kingdom
    Neurosci Lett 444:195-8. 2008
    ..Demyelination in MS is associated with increased activity of MPO, suggesting that this production of reactive oxygen species may contribute to axonal injury within plaques...
  42. doi Immunocapture-based fluorometric assay for the measurement of insulin-degrading enzyme activity in brain tissue homogenates
    James Scott Miners
    Dementia Research Group, Institute of Clinical Neurosciences, Clinical Science at North Bristol, University of Bristol, Bristol BS16 1LE, UK
    J Neurosci Methods 169:177-81. 2008
    ..This assay should allow the measurement of IDE enzyme levels in a variety of biological tissues and may be useful in study of diseases such as Alzheimer's disease and insulin-dependent diabetes...
  43. pmc Distribution and expression of picalm in Alzheimer disease
    Shabnam Baig
    Institute of Clinical Neurosciences, University of Bristol, Frenchay Hospital, Bristol, United Kingdom
    J Neuropathol Exp Neurol 69:1071-7. 2010
    ..Further research is needed to determine whether PICALM expression is influenced by Aβ levels and whether it affects Aβ uptake and transport by endothelial cells...
  44. doi Neprilysin protects against cerebral amyloid angiopathy and Aβ-induced degeneration of cerebrovascular smooth muscle cells
    James Scott Miners
    Dementia Research Group, School of Clinical Sciences, Institute of Clinical Neurosciences, University of Bristol, UK
    Brain Pathol 21:594-605. 2011
    ..Our findings suggest that NEP protects CVSMCs from Aβ toxicity and protects cerebral blood vessels from the development and complications of CAA...
  45. ncbi Phosphorylated Smad 2/3 colocalizes with phospho-tau inclusions in Pick disease, progressive supranuclear palsy, and corticobasal degeneration but not with alpha-synuclein inclusions in multiple system atrophy or dementia with Lewy bodies
    Katy A Chalmers
    Dementia Research Group, University of Bristol Institute of Clinical Neurosciences, Department of Clinical Science at North Bristol, Frenchay Hospital, Bristol, BS16 1LE, UK
    J Neuropathol Exp Neurol 66:1019-26. 2007
    ....
  46. ncbi Protein and gene expression of tumour necrosis factor receptors I and II and their promoter gene polymorphisms in Alzheimer's disease
    Doris Culpan
    Dementia Research Group, Institute of Clinical Neurosciences, Department of Clinical Sciences at North Bristol, University of Bristol, Frenchay Hospital, Frenchay, Bristol, United Kingdom
    Exp Gerontol 42:538-44. 2007
    ..Our findings suggest that TNF-RI and -RII promoter gene polymorphisms and variations in protein and gene expression of these receptors are unlikely to play a major role in the development of AD...
  47. ncbi Endothelin-converting enzyme-1 activity, endothelin-1 production, and free radical-dependent vasoconstriction in Alzheimer's disease
    Jennifer C Palmer
    University of Bristol, Dementia Research Group, Frenchay Hospital, Bristol, UK
    J Alzheimers Dis 36:577-87. 2013
    ..Our findings indicate that cerebral vasoconstriction induced by Aβ results in part from a free radical-mediated increase in ECE-1 activity and ET-1 production. ..
  48. doi Influence of LRP-1 and apolipoprotein E on amyloid-β uptake and toxicity to cerebrovascular smooth muscle cells
    Wan Adriyani W Ruzali
    Dementia Research Group, Institute of Clinical Neurosciences, School of Clinical Sciences, University of Bristol, Frenchay Hospital, Bristol, UK
    J Alzheimers Dis 33:95-110. 2013
    ..This may contribute to the differential effects of APOE genotype on severity of CAA and the risk of rupture of Aβ-laden blood vessels...
  49. pmc CNS SIRT3 expression is altered by reactive oxygen species and in Alzheimer's disease
    Heather J M Weir
    School of Biochemistry, University of Bristol, Bristol, United Kingdom
    PLoS ONE 7:e48225. 2012
    ..Thus, our data suggest a role for SIRT3 in mechanisms sensing and tackling ROS- and AD-mediated mitochondrial stress...
  50. ncbi LRP1 expression in cerebral cortex, choroid plexus and meningeal blood vessels: relationship to cerebral amyloid angiopathy and APOE status
    Wan Adriyani W Ruzali
    Dementia Research Group, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol, BS16 1LE, UK
    Neurosci Lett 525:123-8. 2012
    ..These findings suggest that APOE may influence the severity of CAA through altered expression of LRP1...
  51. ncbi Measurement of pre- and post-synaptic proteins in cerebral cortex: effects of post-mortem delay
    Lai Khai Siew
    Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology Care of the Elderly, University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK
    J Neurosci Methods 139:153-9. 2004
    ..The more robust stability of synaptophysin may be related to its multi-transmembrane structure...
  52. doi Activators and inhibitors of the plasminogen system in Alzheimer's disease
    Rachel Barker
    Dementia Research Group, Institute of Clinical Neurosciences, Clinical Sciences at North Bristol, Bristol University, Bristol, UK
    J Cell Mol Med 16:865-76. 2012
    ..The increases in tPA, uPA, PAI-1 and α2-antiplasmin may counteract each other so that plasmin activity is not significantly altered in AD, but increased tPA may also affect synaptic plasticity, excitotoxic neuronal death and apoptosis...
  53. doi Clinicopathological review of patients with and without multiple sclerosis treated by partial sensory rhizotomy for medically refractory trigeminal neuralgia: a 12-year retrospective study
    Kumar Abhinav
    Department of Neurosurgery, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK
    Clin Neurol Neurosurg 114:361-5. 2012
    ..We have examined the relationship between pathology and treatment outcome in patients with and without MS, treated for intractable TN by partial sensory rhizotomy (PSR)...
  54. doi Clusterin mRNA and protein in Alzheimer's disease
    Shabnam Baig
    Dementia Research Group, Institute of Clinical Neurosciences, University of Bristol, Frenchay Hospital, Bristol, UK
    J Alzheimers Dis 28:337-44. 2012
    ..The increase in clusterin noted in peripheral blood in AD may reflect increased passage of this chaperone protein across the blood-brain barrier but further work is needed to determine how CLU variants influence the development of AD...
  55. doi Characterisation of two antibodies to oligomeric Abeta and their use in ELISAs on human brain tissue homogenates
    Zoë van Helmond
    Dementia Research Group, Institute of Clinical Neurosciences, Clinical Science at North Bristol, University of Bristol, Bristol BS16 1LE, UK
    J Neurosci Methods 176:206-12. 2009
    ..The development of a simple ELISA for measurement of oligomeric Abeta should facilitate further studies of the role of oligomeric species of Abeta in AD...
  56. ncbi APOE promoter, ACE1 and CYP46 polymorphisms and beta-amyloid in Alzheimer's disease
    Katy A Chalmers
    University of Bristol, Department of Care of the Elderly, Frenchay Hospital, Bristol BS16 1LE, UK
    Neuroreport 15:95-8. 2004
    ..Here we report that polymorphisms within the APOE promoter, ACE1 and CYP46 gene are not risk factors for AD and are not associated with parenchymal or vascular accumulation of Abeta...
  57. ncbi Loss of perineuronal net N-acetylgalactosamine in Alzheimer's disease
    Shabnam Baig
    Department of Clinical Science at North Bristol, Care of the Elderly, Frenchay Hospital, University of Bristol, Bristol, UK
    Acta Neuropathol 110:393-401. 2005
    ..This could in turn lead to increased activity of the glutamatergic and other neurons onto which they synapse...
  58. doi Distribution of the branched chain aminotransferase proteins in the human brain and their role in glutamate regulation
    Jonathon Hull
    Faculty of Health and Life Sciences, University of the West of England, Bristol, UK
    J Neurochem 123:997-1009. 2012
    ....
  59. doi Abeta-degrading enzymes in Alzheimer's disease
    James Scott Miners
    Dementia Research Group, University of Bristol Institute of Clinical Neurosciences, Frenchay Hospital, Bristol, UK
    Brain Pathol 18:240-52. 2008
    ....
  60. ncbi Neurofibrillary tangles may interfere with Smad 2/3 signaling in neurons
    Katy A Chalmers
    Dementia Research Group, University of Bristol Institute of Clinical Neurosciences, Department of Clinical Science at North Bristol, Frenchay Hospital, Bristol, UK
    J Neuropathol Exp Neurol 66:158-67. 2007
    ..Interference with the Smad signaling may adversely affect survival of tangle-bearing neurons in AD...
  61. ncbi Immunocapture-based fluorometric assay for the measurement of neprilysin-specific enzyme activity in brain tissue homogenates and cerebrospinal fluid
    James Scott Miners
    Dementia Research Group, Institute of Clinical Neurosciences, Clinical Science at North Bristol, University of Bristol, Frenchay Hospital, Frenchay, Bristol BS16 1LE, UK
    J Neurosci Methods 167:229-36. 2008
    ..The assay allows high-throughput analysis and, critically, also ensures a high level of enzyme specificity even when assaying crude tissue homogenates or CSF...
  62. doi Accumulation of insoluble amyloid-β in down's syndrome is associated with increased BACE-1 and neprilysin activities
    James Scott Miners
    Dementia Research Group, Institute of Clinical Neurosciences, University of Bristol, Bristol, UK
    J Alzheimers Dis 23:101-8. 2011
    ..These findings provide strong support that BACE-1 and NEP activities, but not ACE, increase in response to the accumulation of insoluble Aβ within the brain...
  63. doi Angiotensins in Alzheimer's disease - friend or foe?
    Patrick G Kehoe
    Dementia Research Group, Institute of Clinical Neurosciences, Department of Clinical Science at North Bristol, University of Bristol, Frenchay Hospital, Bristol BS16 1LE, UK
    Trends Neurosci 32:619-28. 2009
    ..This paper reviews molecular, genetic, experimental and clinical data as well as the therapeutic opportunities that relate to the involvement of the RAS in AD...
  64. ncbi Decreased expression and activity of neprilysin in Alzheimer disease are associated with cerebral amyloid angiopathy
    James Scott Miners
    Dementia Research Group, Institute of Clinical Neurosciences, Clinical Science at North Bristol, University of Bristol, Frenchay Hospital, Frenchay, Bristol, United Kingdom
    J Neuropathol Exp Neurol 65:1012-21. 2006
    ..However, logistic regression analysis showed low NEP levels to be a significant independent predictor of moderate to severe CAA...
  65. doi Disease-responsive neural precursor cells are present in multiple sclerosis lesions
    Heidi Snethen
    Department of Neurology, University of Bristol Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS161LE, UK
    Regen Med 3:835-47. 2008
    ..Spontaneous tissue repair occurs in multiple sclerosis (MS), but the origin of remyelinating cells remains obscure. Here we explore the hypothesis that endogenous neural precursors are involved in MS disease processes...
  66. pmc The influence of tumour necrosis factor- α (TNF-α) on amyloid-β (Aβ)-degrading enzymes in vitro
    Doris Culpan
    Dementia Research Group, School of Clinical Sciences, University of Bristol, John James Building, Frenchay Hospital Bristol, BS16 1LE, United Kingdom
    Int J Mol Epidemiol Genet 2:409-15. 2011
    ..In conclusion, apart from a transient reduction in ECE-2 protein levels, TNF-α had no impact in our in vitro experimental system on transcription or translation of any of our selected mediators of Aβ degradation...
  67. ncbi Central demyelination of the Vth nerve root in trigeminal neuralgia associated with vascular compression
    S Love
    Department of Neuropathology, Frenchay Hospital, Bristol, UK
    Brain Pathol 8:1-11; discussion 11-2. 1998
    ..The partly aberrant nature of the myelination within the region of vascular compression may contribute to the persistence of symptoms in some patients after decompressive surgery...
  68. doi Endothelin receptor antagonists: potential in Alzheimer's disease
    Jennifer Palmer
    Dementia Research Group, Institute of Clinical Neurosciences, School of Clinical Sciences, University of Bristol, Frenchay Hospital, Bristol BS16 1LE, United Kingdom
    Pharmacol Res 63:525-31. 2011
    ....
  69. doi Plasminogen and plasmin in Alzheimer's disease
    Rachel Barker
    Dementia Research Group, Institute of Clinical Neurosciences, Clinical Sciences at North Bristol, Bristol University, Bristol, UK
    Brain Res 1355:7-15. 2010
    ..Plasmin activity was reduced in AD but this did not reach statistical significance. In contrast to some studies these data do not support the involvement of plasmin in the abnormal accumulation of Aβ in AD...
  70. ncbi Abeta-related angiitis: primary angiitis of the central nervous system associated with cerebral amyloid angiopathy
    Neil J Scolding
    Department of Neurology, Institute of Clinical Neurosciences, University of Bristol, Frenchay Hospital, Bristol, UK
    Brain 128:500-15. 2005
    ....
  71. ncbi Contributors to white matter damage in the frontal lobe in Alzheimer's disease
    K Chalmers
    University of Bristol, Department of Clinical Science, Frenchay Hospital, Bristol, UK
    Neuropathol Appl Neurobiol 31:623-31. 2005
    ..008). Our findings suggest that severity of frontal white matter damage in AD is closely related to parenchymal Abeta load and that in most cases the contribution of degenerative vascular disease, CAA and APOE is relatively minor...
  72. ncbi Inter-laboratory comparison of DNA preservation in archival paraffin-embedded human brain tissue from participating centres on four continents
    S Kösel
    Department of Neuropathology, Imperial College School of Medicine, London, UK
    Neurogenetics 3:163-70. 2001
    ....
  73. doi Low-temperature improved-throughput method for analysis of brain fatty acids and assessment of their post-mortem stability
    Thomas Fraser
    Dementia Research Group, Institute of Clinical Neurosciences, Clinical Science at North Bristol, University of Bristol, Frenchay Hospital, Frenchay, Bristol BS16 1LE, UK
    J Neurosci Methods 169:135-40. 2008
    ..The development of this method and the observation that delay of up to 3 days has no effect on fatty acid content will facilitate further studies of fatty acid composition on large cohorts of post-mortem brains...
  74. pmc Tumour necrosis factor-α (TNF-α) and miRNA expression in frontal and temporal neocortex in Alzheimer's disease and the effect of TNF-α on miRNA expression in vitro
    Doris Culpan
    Dementia Research Group, School of Clinical Sciences, University of Bristol, John James Buildings, Frenchay Hospital Frenchay, Bristol, BS16 1LE, United Kingdom
    Int J Mol Epidemiol Genet 2:156-62. 2011
    ..Our brain tissue findings argue against a role for TNF-α in influencing the expression of these miRNAs in AD...
  75. ncbi Late-onset hereditary sensory neuropathy type I due to SPTLC1 mutation: autopsy findings
    Andrea J Lindahl
    Department of Neurology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK
    Clin Neurol Neurosurg 108:780-3. 2006
    ..We report the neuropathological findings in a 93-year-old woman with a disease of unusually late onset, who was part of a large HSN I kindred and in whom genetic analysis confirmed an SPTLC1 T399G mutation...
  76. ncbi Epilepsy surgery for refractory epilepsy due to encephalocele: a case report and review of the literature
    Howard J Faulkner
    Department of Neurology, Frenchay Hospital, North Bristol NHS Trust, Bristol, United Kingdom
    Epileptic Disord 12:160-6. 2010
    ..Epilepsy patterns associated with encephalocele and their management are reviewed...
  77. ncbi Relationship of neurofibrillary pathology to cerebral amyloid angiopathy in Alzheimer's disease
    S Williams
    Care of the Elderly, Institute of Clinical Neurosciences, Department of Clinical Science at North Bristol, University of Bristol, Bristol, UK
    Neuropathol Appl Neurobiol 31:414-21. 2005
    ..We propose that both CAA and peri-vascular accumulation of hyperphosphorylated tau may be a consequence of elevated levels of soluble A beta around cortical arteries and arterioles...
  78. doi Tau hyperphosphorylation affects Smad 2/3 translocation
    S Baig
    Dementia Research Group, Institute of Clinical Neurosciences, Department of Clinical Science at North Bristol, University of Bristol, Frenchay Hospital, Bristol BS16 1LE, UK
    Neuroscience 163:561-70. 2009
    ..This may compromise neuroprotective actions of TGFbeta and contribute to neurodegeneration in AD...
  79. ncbi MMP-2, -3 and -9 levels and activity are not related to Abeta load in the frontal cortex in Alzheimer's disease
    S Baig
    Dementia Research Group, Institute of Clinical Neurosciences, Department of Clinical Science at North Bristol, University of Bristol, Frenchay Hospital, Bristol, UK
    Neuropathol Appl Neurobiol 34:205-15. 2008
    ..Our findings suggest that altered expression of these proteases does not make a significant contribution to the accumulation of Abeta in AD...
  80. ncbi Familial idiopathic brain calcification--a new and familial alpha-synucleinopathy?
    Samden D Lhatoo
    Department of Neurology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol, UK
    Eur Neurol 49:223-6. 2003
    ..This may represent a new and familial alpha-synuclein disorder causing a predominantly extrapyramidal picture similar to multisystem atrophy...
  81. ncbi Surgical intervention, biopsy and APOE genotype in cerebral amyloid angiopathy-related haemorrhage
    M O McCarron
    Department of Neuropathology, Southern General Hospital, Glasgow, UK
    Br J Neurosurg 13:462-7. 1999
    ..Despite surgical intervention, CAAH has a poor outcome in patients with impaired consciousness. Clinical awareness of CAAH and use of A beta immunostaining may increase the diagnostic yield from cerebral biopsy...
  82. ncbi Transforming growth factor-betas in a rat model of neonatal posthaemorrhagic hydrocephalus
    S Cherian
    Department of Clinical Science South Bristol, University of Bristol, Bristol, UK
    Neuropathol Appl Neurobiol 30:585-600. 2004
    ....
  83. ncbi APOE epsilon 4 influences the pathological phenotype of Alzheimer's disease by favouring cerebrovascular over parenchymal accumulation of A beta protein
    K Chalmers
    Department of Care of the Elderly, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol, UK
    Neuropathol Appl Neurobiol 29:231-8. 2003
    ..These findings indicate that possession of the APOE epsilon 4 allele favours vascular over parenchymal accumulation of A beta in AD. This may influence the pathogenesis of neurodegeneration in epsilon 4-associated AD...
  84. ncbi Caveolin-1 and -2 and their relationship to cerebral amyloid angiopathy in Alzheimer's disease
    Z K van Helmond
    Dementia Research Group, Institute of Clinical Neurosciences, Clinical Science at North Bristol, University of Bristol, Frenchay Hospital, Bristol, UK
    Neuropathol Appl Neurobiol 33:317-27. 2007
    ..Our findings suggest that alterations in the expression of vascular CAV-1 and CAV-2 are unlikely to play a role in the development of CAA in AD...
  85. ncbi Angiotensin-converting enzyme (ACE) levels and activity in Alzheimer's disease, and relationship of perivascular ACE-1 to cerebral amyloid angiopathy
    J S Miners
    Dementia Research Group, Institute of Clinical Neurosciences, Clinical Science at North Bristol, University of Bristol, Frenchay Hospital, Frenchay, Bristol, UK
    Neuropathol Appl Neurobiol 34:181-93. 2008
    ..We analysed ACE-1 activity and expression in AD and control brains, particularly in relation to Abeta load and cerebral amyloid angiopathy (CAA)...
  86. ncbi Involvement of apolipoprotein E in herpes simplex encephalitis
    J A Nicoll
    Department of Neuropathology, University of Glasgow, Institute of Neurological Sciences, Southern General Hospital, UK
    Neuroreport 12:695-8. 2001
    ..We conclude that apoE is involved in the response to damage associated with HSE, as in other forms of brain injury. However, APOE genotype does not appear to influence either the risk of developing HSE or subsequent mortality...
  87. ncbi Damage to intracranial optic pathways in fatal closed head injury in man
    B Perunovic
    Department of Neuropathology, Frenchay Hospital, Bristol BS161LE, UK
    J Neurol Sci 185:55-62. 2001
    ..The findings suggest that damage to the posterior parts of the optic pathways may be under-diagnosed among patients with head injury...
  88. ncbi Sequence variants of IDE are associated with the extent of beta-amyloid deposition in the Alzheimer's disease brain
    Mia E L Blomqvist
    Center for Genomics and Bioinformatics, Karolinska Institute, Stockholm, Sweden
    Neurobiol Aging 26:795-802. 2005
    ..Results indicate that alleles of IDE contribute to variability in A beta deposition in the AD brain and suggest that this relationship may have relevance for the degree of cognitive dysfunction in AD patients...
  89. doi Long-term effects of Abeta42 immunisation in Alzheimer's disease: follow-up of a randomised, placebo-controlled phase I trial
    Clive Holmes
    Division of Clinical Neurosciences, University of Southampton, Southampton, UK Moorgreen Hospital, Hampshire Partnership Trust, Southampton, UK
    Lancet 372:216-23. 2008
    ..Our aim was to assess the relation between Abeta(42) immune response, degree of plaque removal, and long-term clinical outcomes...
  90. ncbi Retrograde reactions of Clarke's nucleus neurons after human spinal cord injury
    Andreas B Schmitt
    Aachen Spinal Cord Research Center, Department of Neurology, University Hospital Aachen, Aachen, Germany
    Ann Neurol 54:534-9. 2003
    ..These results support experimental data that nonregenerating central nervous system neurons can temporarily upregulate regeneration-associated genes, reflecting a transient regenerative capacity that fails over time...
  91. ncbi Unilateral subthalamotomy in the treatment of Parkinson's disease
    Nikunj K Patel
    Institute of Clinical Neurosciences, Frenchay Hospital, Bristol, UK
    Brain 126:1136-45. 2003
    ..Com bined lesioning of the dorsolateral STN and H2/ZI is particularly effective...
  92. doi Clearance of Abeta from the brain in Alzheimer's disease. Foreword
    Seth Love
    Brain Pathol 18:239. 2008
  93. ncbi Genetic variants of ABCA1 modify Alzheimer disease risk and quantitative traits related to beta-amyloid metabolism
    Hagit Katzov
    Center for Genomics and Bioinformatics, Karolinska Institute, Stockholm, Sweden
    Hum Mutat 23:358-67. 2004
    ..Results indicate that variants of ABCA1 may affect the risk of AD, providing further support for a genetic link between AD and cholesterol metabolism...
  94. ncbi MRI-directed subthalamic nucleus surgery for Parkinson's disease
    Nikunj K Patel
    Institute of Clinical Neurosciences, Frenchay Hospital, Bristol, UK
    Stereotact Funct Neurosurg 78:132-45. 2002
    ....
  95. ncbi Glial cell line-derived neurotrophic factor induces neuronal sprouting in human brain
    Seth Love
    Nat Med 11:703-4. 2005