I studied Medicine at the University of Birmingham (1991-97) and continued my general medical training in Oxford. I then spent three years working on the genetic linkage and association of neurological disorders at the Wellcome Trust Centre for Human Genetics. After obtaining my DPhil in 2003, I completed my training in Clinical Neurology at Oxford. I joined the Department of Physiology, Anatomy and Genetics in 2007 after being awarded an MRC Clinician Scientist Fellowship to establish my own research group. I then led IMI StemBANCC - an large public-private partnerhsip funded by the EU to establish iPSC resources for academia and industry across europe.
I now lead IMI IM2PACT which is an amibitious research programme to investigate disease mechanism involving the brain neurovascular unit and find transport mechanisms to get therapeutics into the brain.
My research group aims to develop resources and tools to improve drug discovery by leveraging human data and human iPSC brain models. We work on pain/migraine, Alzheimer's disease and autism/epilepsy.
I am also active clinically and work as a Consultant Neurologist at the John Radcliffe Hospital with an interest in Headache Disorders. I am Director of the Oxford Headache Centre and developed the Oxford Community Headache Service.
Director of the Oxford Headache Centre and Director of StemBANCC
- Professor of Neuroscience and Neurology
- Consultant Neurologist
Molecular disease mechanisms and cellular disease phenotypes in neurological disorders
The Translational Molecular Neuroscience Group looks at neurogenetic disorders, often rare variants of common disease. Understanding the disease pathways in these conditions will allow development of meaningful therapies. The group is developing new disease models for more effective drug discovery platforms.
Sources of Funding
- EU FP7
- Wellcome Trust
- NIHR BRC
- Medical Research Council
- John Fell
Aneuploidy effects on human gene expression across three cell types.
Liu S. et al, (2023), Proc Natl Acad Sci U S A, 120
A novel human iPSC model of COL4A1/A2 small vessel disease unveils a key pathogenic role of matrix metalloproteinases in extracellular matrix abnormalities
Al-Thani M. et al, (2023)
Mathematical modelling of brain mTOR activity identifies selective vulnerability of cell types and signalling pathways
Pokhilko A. et al, (2022)
Lipopolysaccharide distinctively alters human microglia transcriptomes to resemble microglia from Alzheimer's disease mouse models.
Monzón-Sandoval J. et al, (2022), Dis Model Mech, 15
Neurons derived from individual early Alzheimer's disease patients reflect their clinical vulnerability.
Ng B. et al, (2022), Brain Commun, 4