Professor of Neurology and Neurobiology
- Senior Wellcome Clinical Scientist
- Honorary Consultant Neurologist
My research aim is to gain a better understanding of the response of the nervous system to injury in order to develop strategies to promote peripheral nerve repair and to prevent the development of neuropathic pain. This is complementary to my clinical interest in peripheral neuropathy and as such links with my specialist neuropathy clinical service at the Oxford University Hospitals. I employ a variety of techniques including cell culture, preclinical transgenic models and transcriptional profiling as well as biomarker, psychophysical and genetic studies in neuropathy patients. This research programme is leading to a better understanding of the signaling events required for effective nerve repair and improved means of patient stratification. I have been involved in understanding the genetic basis of inherited painful channelopathies (for instance familial episodic pain syndrome due to TRPA1 mutations) and in the description and validation of novel pain mediators such as NGF and CXCL5. In the case of NGF a monoclonal antibody aimed at this factor has shown efficacy in phase 3 clinical trials. I am a member of the London Pain Consortium, a PI on the Innovative Medicines Initiatives ‘Stembancc’ and I am vice director of the ‘Europain’ IMI project.
DOLORisk: study protocol for a multi-centre observational study to understand the risk factors and determinants of neuropathic pain
Pascal M. et al, (2018), Wellcome Open Research
Hereditary sensory neuropathy type 1-associated deoxysphingolipids cause neurotoxicity, acute calcium handling abnormalities and mitochondrial dysfunction in vitro.
Wilson ER. et al, (2018), Neurobiol Dis, 117, 1 - 14
Neuropathic pain drives anxiety behavior in mice, results consistent with anxiety levels in diabetic neuropathy patients.
Sieberg CB. et al, (2018), Pain Rep, 3
Rare NaV1.7 variants associated with painful diabetic peripheral neuropathy.
Blesneac I. et al, (2018), Pain, 159, 469 - 480
Immune or Genetic-Mediated Disruption of CASPR2 Causes Pain Hypersensitivity Due to Enhanced Primary Afferent Excitability.
Dawes JM. et al, (2018), Neuron, 97, 806 - 822.e10