Kevin Talbot qualified in medicine (MB BS) with Distinction from the University of London and trained in Neurology in London and Oxford. He joined the laboratory of Professor Kay Davies in 1995 to work on the childhood motor neuron disorder spinal muscular atrophy, which has remained a major focus of his research ever since. From 1998-2001 he was Clinical Lecturer in Neurology and from 2001-2006 held an MRC Clinician Scientist Fellowship. He leads a multidisciplinary team providing a clinical service for patients with motor neuron disease from all over the South of England. In 2010 he became Professor of Motor Neuron Biology
Awards, Training and Qualifications
- MB BS University of London 1990
- DPhil University of Oxford 1998
- FRCP Royal College of Physicians, London 2006
MB BS, DPhil, FRCP
Head of Clinical Neurology and Professor of Motor Neuron Biology
The main aim of my research is to identify targets for therapy in motor neuron diseases such as amyotrophic lateral sclerosis and spinal muscular atrophy. In particular, we use laboratory models including motor neurons from induced pluripotent stem cells from patients to understand why motor neuron integrity fails in the presence of certain genetic mutations (eg; TDP-43 or C9orf72 in ALS). We also use these models to identify drug targets. Our work takes place in the context of a larger team of researchers in Oxford interested in translational research in neurodegenerative diseases, and we have many national and international collaborations.
Single-copy expression of an amyotrophic lateral sclerosis-linked TDP-43 mutation (M337V) in BAC transgenic mice leads to altered stress granule dynamics and progressive motor dysfunction
Gordon D. et al, (2019), Neurobiology of Disease, 121, 148 - 162
ALS-associated missense and nonsense TBK1 mutations can both cause loss of kinase function.
de Majo M. et al, (2018), Neurobiol Aging, 71, 266.e1 - 266.e10
Towards a TDP-43-Based Biomarker for ALS and FTLD.
Feneberg E. et al, (2018), Mol Neurobiol, 55, 7789 - 7801
Neurodegeneration in SCA14 is associated with increased PKCγ kinase activity, mislocalization and aggregation.
Wong MMK. et al, (2018), Acta Neuropathol Commun, 6
Frequency and signature of somatic variants in 1461 human brain exomes.
Wei W. et al, (2018), Genet Med