Dr Owain Howell

Publications

Journal Articles

  1. & (2019). Using biomarkers to predict clinical outcomes in multiple sclerosis. Practical Neurology 19(4), 342-349.
  2. & (2019). Calorie restriction activates new adult born olfactory‐bulb neurones in a ghrelin‐dependent manner but acyl‐ghrelin does not enhance subventricular zone neurogenesis. Journal of Neuroendocrinology 31(7)
  3. & (2018). Meningeal inflammation and cortical demyelination in acute multiple sclerosis. Annals of Neurology
  4. & (2018). Molecular pathology of Multiple Sclerosis lesions reveals a heterogeneous expression pattern of genes involved in oligodendrogliogenesis. Experimental Neurology
  5. & (in press). Inflammatory intrathecal profiles and cortical damage in multiple sclerosis. Annals of Neurology
  6. & (2018). Measurement of soluble CD59 in CSF in demyelinating disease: Evidence for an intrathecal source of soluble CD59. Multiple Sclerosis Journal
  7. & (2017). Tissue microarray methodology identifies complement pathway activation and dysregulation in progressive multiple sclerosis. Brain Pathology
  8. & (2016). Complement is activated in progressive multiple sclerosis cortical grey matter lesions. Journal of Neuroinflammation 13(1)
  9. & (2015). Extensive grey matter pathology in the cerebellum in multiple sclerosis is linked to inflammation in the subarachnoid space. Neuropathology and Applied Neurobiology 41(6), 798-813.
  10. & (2014). Complement activation in multiple sclerosis plaques: an immunohistochemical analysis. Acta Neuropathologica Communications 2(1), 53
  11. & (2013). Cortical grey matter demyelination can be induced by elevated pro-inflammatory cytokines in the subarachnoid space of MOG-immunized rats. Brain
  12. & (2012). Meningeal inflammation plays a role in the pathology of primary progressive multiple sclerosis. Brain 135(10), 2925-2937.
  13. & (2011). Meningeal inflammation is widespread and linked to cortical pathology in multiple sclerosis. Brain 134(9), 2755-2771.
  14. & (2011). The neuropathological basis of clinical progression in multiple sclerosis. Acta Neuropathologica 122(2), 155-170.
  15. & (2011). Mitochondrial DNA deletions and neurodegeneration in multiple sclerosis. Annals of Neurology 69(3), 481-492.
  16. & (2011). Related B cell clones populate the meninges and parenchyma of patients with multiple sclerosis. Brain 134(2), 534-541.
  17. & (2010). Two binding sites for [3H]PBR28 in human brain: implications for TSPO PET imaging of neuroinflammation. Journal of Cerebral Blood Flow & Metabolism 30(9), 1608-1618.
  18. & (2010). A Gradient of neuronal loss and meningeal inflammation in multiple sclerosis. Annals of Neurology 68(4), 477-493.
  19. & (2010). HDAC1 nuclear export induced by pathological conditions is essential for the onset of axonal damage. Nature Neuroscience 13(2), 180-189.
  20. & (2010). Activated Microglia Mediate Axoglial Disruption That Contributes to Axonal Injury in Multiple Sclerosis. Journal of Neuropathology and Experimental Neurology 69(10), 1017-1033.
  21. & (2010). Detection of Epstein-Barr virus and B-cell follicles in the multiple sclerosis brain: what you find depends on how and where you look. Brain 133(12), e157-e157.
  22. & (2007). NPY mediates basal and seizure-induced proliferation in the subcallosal zone. NeuroReport 18(10), 1005-1008.
  23. & (2007). Neuropeptide Y is important for basal and seizure-induced precursor cell proliferation in the hippocampus. Neurobiol Disease 26, 174
  24. & (2006). Meningeal B-cell follicles in secondary progressive multiple sclerosis associate with early onset of disease and severe cortical pathology. Brain 130(4), 1089-1104.
  25. & (2006). Disruption of neurofascin localization reveals early changes preceding demyelination and remyelination in multiple sclerosis. Brain 129(12), 3173-3185.
  26. & (2003). Sedation and Anesthesia Mediated by Distinct GABAA Receptor Isoforms. J Neurosci 23, 8607-8617.
  27. et. al. (2003). Sedation and Anesthesia Mediated by Distinct GABAAReceptor Isoforms. The Journal of Neuroscience 23(24), 8608-8617.
  28. & (2002). Enhanced Learning and Memory and Altered GABAergic Synaptic Transmission in Mice Lacking the α5 Subunit of the GABAAReceptor. J Neurosci 22, 5572
  29. & (2002). Enhanced Learning and Memory and Altered GABAergic Synaptic Transmission in Mice Lacking the α5 Subunit of the GABAAReceptor. The Journal of Neuroscience 22(13), 5572-5580.
  30. & (2001). Loss of the Major GABAA Receptor Subtype in the Brain Is Not Lethal in Mice. J Neurosci 21, 3409-3418.
  31. & (2001). Loss of the Major GABAAReceptor Subtype in the Brain Is Not Lethal in Mice. The Journal of Neuroscience 21(10), 3409-3418.
  32. & (2000). Density and pharmacology of α5 subunit-containing GABAA receptors are preserved in hippocampus of Alzheimer’s disease patients. Neuroscience 98, 669-675.
  33. & (2000). Sedative but not anxiolytic properties of benzodiazepines are mediated by the GABAA receptor alpha1 subtype. Nature Neuroscience 3, 587-592.
  34. & (2000). Changes in [3H]zolpidem and [3H]Ro 15-1788 binding in rat globus pallidus and substantia nigra pars reticulata following a nigrostriatal tract lesion.. Brain Res 862, 280
  35. & (2000). Changes in [3H]zolpidem and [3H]Ro 15-1788 binding in rat globus pallidus and substantia nigra pars reticulata following a nigrostriatal tract lesion. Brain Research 862(1-2), 280-283.
  36. & (2000). Density and pharmacology of α5 subunit-containing GABAA receptors are preserved in hippocampus of Alzheimer’s disease patients. Neuroscience 98(4), 669-675.
  37. & (1999). Autoradiographic localization of α5 subunit-containing GABAA receptors in rat brain. Brain Res 822, 265
  38. & (1999). Autoradiographic localization of α5 subunit-containing GABAA receptors in rat brain. Brain Research 822(1-2), 265-270.