Dr. Simon Stott has been working in the field of Parkinson’s disease research for over 15 years (both in academia and biotech). He is currently a research associate in the department of Clinical Neuroscience at the University of Cambridge, in Prof. Roger Barker’s lab. He also runs the incredibly informative blog, The Science Of Parkinson’s.
The following has been paraphrased from an interview with Dr. Simon Stott on November 28th, 2017.
(Full audio version)
Surely you have enough on your plate with all of your lab work, what compelled you to spend so much more time communicating the science of PD?
About 3 years ago I started getting involved in the clinic here at Cambridge. I realized after 10 years of studying the disease that I hadn’t spent much time with the condition itself. It was an eye-opening experience. Through it I realized there was an enormous thirst for information and people were going to strange places to try and find that information. I felt a responsibility to put information out there that was easy to read and understand to try and steer the community away from some of the darker places on the internet where people go looking for information.
What do you find to be the most frustrating aspects of trying to communicate science to the public?
The way a lot of what I say gets taken out of context. I am relatively optimistic, I think that within my daughter’s lifetime we are going to make significant progress to the point where this condition won’t be such a problem for them. But readers often take that and contact my boss saying ‘Simon said we are going to cure Parkinson’s tomorrow’.
There is a need in the media to simplify these incredibly complex issues, but in doing so they create a lot of misinformation and over-exaggerated claims. Do you think they ultimately help or hurt the community?
The mass media needs to look itself in the mirror. The things that we are investigating are getting more and more complex and we have to provide people with more information than what mass media gives. There is a desperate need to bridge the gap between complicated research articles and the crazy headlines that most people see.
People themselves also need to seek second opinions, even for information found on my site. Einstein himself said that we don’t go from fact to fact, we go from assumption to assumption with science. A lot of the research relates to groups of people, not individuals, in that regard everyone needs to be very proactive and find out as much about themselves as they can. A lot of what you hear in the media might not relate to you yourself.
What do you make of recent attempts to introduce cellular scaffolding to cell replacement therapy and do you know if this is something people working on these techniques are considering? (Source)
Taking anything to a clinic takes such a long time, getting cell transplantation in particular past all the regulators is such an ordeal, that if you add anything else to the process it would only delay the therapy. Protocols need to be rigorously tested and any changes made to the process would add an extra level of complexity. The research is very exciting, but it is too complicated to introduce anything new to the transplantation therapies we are working on. In the far future we might be able to add them.
Why is it so difficult for us to study the effects of more than one factor at a time? Living biological systems have multiple factors interacting at any given time, shouldn’t our studies try to do the same?
Just looking at one factor is extremely complicated. If you have a particular genetic mutation you are looking at you see different phenotypes(observable characteristics) between different strains of mice. In one strain the mutation might be lethal, in another it might make them hyperactive. But there is a push to looking at multifactorial approaches, especially in these new adaptive clinical trials. The I-Spy program for cancer is a good example. The hope would be that we try something similar with PD, but it is a great challenge.
Take an individual protein, it does different things at different times in a cell. It will have one function at one particular stage of cell division and a different function at a different stage of cell division. Then if you change to a different type of cell it will exhibit completely different functions. We want to look at things at a multifactorial basis but it is still extremely complicated.
Do you believe alpha-synuclein is a cause or effect of Parkinson’s disease?
While I hope that it is a cause because we have all these clinic trials going on targeting it, I think the community needs to prepare itself that it isn’t that simple. The brain is so complicated, I seriously doubt that it comes down to one protein. If it really was that simple then we would probably be too simple to understand it.
How many different types of PD do you suspect there are and where do you see the best attempts being made to create sub-types of PD?
I think Parkinson’s is a syndrome of multiple conditions that exhibit similar biological outputs. But the commonalities are interesting, why is it that a lady up in Edinburgh can smell Parkinson’s? What is it that people with Parkinson’s share that allows her to smell it?
We have an interesting study in the lab at the moment that allows us to use breath to examine the disease. It may give us some interesting new bio-markers that could lead to new sub-types.
Genetics is the most interesting area for me. There are new genetic variants popping up all the time that allow us to identify some of the differences that we do see, though they also point to similar biological processes going on inside the cell.
What are the biggest barriers that stand in the way of progress and what changes do you hope to see to how science is done over your career?
Funding and regulation of course stand in the way, but to give a less obvious answer I’d say imagination. In science it is very easy for everyone to go chasing after the same topics, as is the case with alpha-synuclein. But we need to be looking at what else is there. Also the short time-frames don’t allow big projects to be done. Could Fred Sanger have done his work in the modern system? I’m not sure.
Also there is the evidence tail wagging the clinical dog scenario. We are making marginal advances based on very small variations to our current stream of evidence. There are very few people taking the big bold reckless steps like Barry Marshall swallowing a petri dish full of bacteria to prove that bacteria in the gut cause ulcers. That sort of spirit has largely disappeared, which is kind of sad.
Having said that there are efforts to counter this. There are groups like the Howard Hughes Institute which give money to the biggest and the best in the research community. They say here is a couple million dollars, do whatever you want. I think that is a fantastic endeavor.
With regards to changes I would like to see, number one would be open access and open data. It infuriates me when I go looking for a paper and it is behind a paywall or you just can’t access it. It would also give more opportunities to citizen researchers. Number two would be more opportunities for career development for younger and mid-level researchers. We are losing good people every year because the incentive structure isn’t there. Science is becoming almost a filtering system for sociopaths like myself. We need a change in the structure to keep these people that have developed an expertise.
For more on Dr. Simon Stott visit The Science Of Parkinson’s.