Kevin Talbot Q & A
Our second SMA scientist under the microscope is Kevin Talbot from the University of Oxford who works both in the clinical and the laboratory.
When I first started seeing patients as a clinical medical student in London, I realised that it was not enough to make a diagnosis and give a treatment. I always found myself thinking about the fundamental reasons why disease occurred in the first place. Before qualifying, I took a year out of clinical training and did a BSc in Molecular Medicine at St Mary’s Hospital in 1989, working on my research project on Alzheimer’s Disease. It was then that I became sure that I wanted a career in neurology which combined seeing patients with researching on the basic molecular aspects of disease.
How did you come to work on SMA?
As so often with these things, it was by chance. In 1993, after I had done post-graduate general medical training and started neurology specialist training, I started looking around for a research position. At that time, and it is still mostly the case, every neurologist did a period of research as part of their training on the way to becoming a Consultant. However, I knew that I wanted to continue research into the future, so looked for the best possible training. I approached a number of scientists in London, Oxford and Cambridge who were prominent in the field of molecular research in neurological disease. It was the era of many new discoveries in genetic disease. I knew that finding the gene was only the first step in understanding the cause of each disease. I wanted to learn how to understand how an error in a gene actually led to a disease through studying models in the laboratory. I met Professor Dame Kay Davies, who suggested that the gene for a disorder called SMA, which I had only barely heard of, was near to being identified. I applied to the Medical Research Council for a research fellowship to work in Kay’s lab and started in November 2004. Within 2 months of my arrival the survival motor neuron (SMN) gene was identified by researchers in France. The next 3 years of my research fellowship were spent trying to understand how mutations in SMN lead to SMA. I have been working on it for most of the last 15 years.
What would you be if you weren’t a scientist/clinician?
Before starting medical school I actually had a place at University to study Mathematics and Theoretical Physics. I wanted to become a particle physicist by working out the fundamental nature of the universe while writing equations on the back of a napkin, sipping espresso in a café on a Paris boulevard. I went travelling and discovered that working out why people got disease was just as interesting.
I am assuming that you will allow me to pretend that I have any artistic talent? A singer of Opera and German Lieder, or perhaps a cellist in a string quartet? I have occasionally fantasised about being an architect, but mainly because they always seem to wear such interesting spectacles. When I was a child I was sure that I would become an MP...in retrospect I think I would not have enjoyed ‘toeing the Party line’.
If you are not In the lab or seeing patients, you are...
Spending time with my children…teenagers need their parents just as a much as toddlers. Reading, going for a run or a walk in the countryside, cooking, travelling for pleasure, going to the opera or concerts. I have sung in a number of choirs over the last decade, but find it very difficult to fit in any kind of regular commitment.
Describe yourself in three words
What has been the most important moment of your career so far?
I think I would have to say getting a secure position in Oxford and the Chair of Motor Neuron Biology recently, which gives me real hope that we can build something in the long term which will lead to new treatments for SMA and other motor neuron disorders.
What Is your most memorable finding relating to SMA?
The most satisfying experiment we have done, and the most complicated, is to use special microchips to look at tissue from an SMA mouse model to see if deficiency of the SMN gene altered splicing. The result went against some received opinion in the field, but I think has now gained acceptance by many researchers. It gets to the heart of why mutations in SMN lead to SMA.
What is your favourite conference location?
Now, I would not wish to give your readers the impression that all scientists do is swan around the world attending conferences. However, I could thoroughly recommend Chicago as a place to spend a bit of time. It has the most wonderful architecture of any modern city in the world, one of the best orchestras, the Chicago Art Institute and the truly magnificent Gibson’s Steak House.
What is the best scientific advice you ever received?
Do not believe someone else’s results, even if they are published in a prestigious scientific journal, if they do not fit the facts. If in doubt, do the experiment yourself.
If you could start your scientific career all over again, are there things you would do differently?
I think that there have been times when I have become interested in too many things at once. I have a tendency to take on too much. It is generally better, and more satisfying, to study one problem in great detail and really understand it. Otherwise, I have very few regrets.
In your opinion, what makes a good scientist?
Most importantly, someone who is willing to think beyond the obvious and to challenge received wisdom. You need the right mixture of meticulous attention to detail and a broad ‘big picture’ vision. These days most successful scientists are also good leaders and are able to motivate people around them. The old image of the solitary scientist hidden away on their own in a basement laboratory is outdated.
Where do you see the SMA research field In the next 10 years?
SMA is a curable disease. It is a question of how to deliver the right therapy to the right place at the right time. We are on the threshold of clinical trials of molecular therapy. While it will not be without some problems, in 10 years time I feel confident that patients with SMA will be treated with therapies that have a real chance of preventing muscle weakness if given early, or at least slowing deterioration.