2011-11-16
On October 31st, at three o’clock in the afternoon, Swedish time, a diverse group of people from all over the world the world sat down in front of their computers, in office chairs or by their kitchen tables, to take part in the first MultiPark webinar on Parkinson’s disease. A multinational grouping - consisting of Swedes, Dutchmen, Brits and Norwegians - had converged to try to cobble together a live broadcast with the goal of sparking a discussion across continents.
The web statistics afterwards suggested that goal had been reached. When the last cameras and microphones had been packed away it was clear that visitors from 124 cities worldwide had taken part in the inaugural webinar.
The headliners of the day were MultiPark’s Patrik Brundin, Angela Cenci-Nilsson and Gesine Paul. The trio’s talks stretched from the excitement and uncertainties of experimental science to the organizing of ongoing trials in cell therapy. In an effort to give life to the age-old seminar set-up each talk was followed by a discussion initiated by questions from the on-stage Parkinson’s Movement panel and the live audience. Before soon online participants were also taking part in the debate, sometimes stumping the scientists with their well-informed questions.
The webinar format inspired a conversation encompassing different actors and groups within the global Parkinson community, giving a voice to all who wanted to engage in the debate. Young scientists were perhaps the most active group on the live chat, while the live audience included many patients with advanced stages of Parkinson’s. Senior researchers were also weighing in on the web discussion and Patrik Brundin, on stage with his laptop comfortably placed in his lap, took upon himself the dual role of interrogator and defendant as he posted comments on the chat while answering increasingly sophisticated questions in front of the cameras.
Patrik Brundin was also the one who kicked of proceedings with his talk on the role of alpha-synuclein in the disease progression of Parkinson’s disease. Professor Brundin has been a pioneer in describing how the mutated protein travels from cell to cell, triggering the slow breakdown of motor neurons in the basal ganglia region of the brain. His working hypothesis is that the misfolding of alpha-synuclein, and the prion like spread of this sick protein, could be what sets of the negative chain of events leading to Parkinson’s disease. The Brundin research group has been able to tie early symptoms of Parkinson’s - such as sleep disorder, loss of sense of smell and constipation – to the development of harmful clumps of aggregated alpha-synuclein in the areas of the brain governing these functions, suggesting that the spread of the sick protein is an important key to understanding the enigma of where Parkinson’s disease may first start.
After his presentation Patrik Brundin was hit with questions from around the world. One question, that always seems to pop up in these settings, and understandably so, was; “When will this research lead to a viable therapy in the clinic?” Professor Brundin answered, somewhat tentatively; “It’s of course difficult to say, we are in the early stages here, but I always say five to ten years because I believe that to be a fair description of what is probable, but the answer is of course that I don’t really know”.
Next to take the stage was Angela Cenci-Nilsson, a world-renowned authority on the role of L-DOPA induced dyskinesia in Parkinson’s disease. She has been a leading presence in the field for a number of years and her research group has been integral in the development of animal models for dyskinesia, helping to move a number of laboratory discoveries to the clinic. Professor Cenci-Nilsson talked to the audience about her latest research targets for reducing L-DOPA induced dyskinesia.
One such target is the effort to block the overactivation of glutamate signals, which have been linked to the development of dyskinesia. The dopamine in our brains fine-tunes the signal strength of important neural circuits and the loss of dopamine in Parkinson’s disease can create an imbalance between these different signal systems. With L-DOPA treatment additional changes occur in this complex neural circuitry. One target for professor Cenci-Nilsson is now to develop a drug that stops the glutamate overactivation by blocking a glutamate receptor called ‘mGluR5’.
“If we can block this glutamate receptor we could prevent the negative effects and improve the dyskinesias resulting from L-DOPA medication. Several clinical trials are now ongoing to evaluate the effects of mGluR5 antagonists in L-DOPA treated PD-patients. Two phase-2 trials have already reported significant positive results”, explained Angela Cenci-Nilsson, before she opened up to questions from the web visitors and the live audience.
The final presentation of the day was delivered by Gesine Paul, a neurologist and scientist who divides her time between the clinic and cell therapy experiments in the lab. Dr Paul talked about the exciting potential that cell transplants could have for Parkinson’s patients. Illustrated by a video from the world famous transplants performed by Olle Lindvall and Anders Björklund in the late 80’s, where a person that has undergone a transplant shows clear motor function improvements years later, she effectively demonstrated the possible impact that this research field still could have for future therapies.
However, the field of cell therapy has always attracted its fair share of skeptics. Ethical issues relating to the use of aborted fetuses as well as doubts concerning the cost effectiveness and logistics of cell therapy are routinely used as arguments for shelving the method as a viable, universal therapy for Parkinson’s patients.
Dr Paul was the first to admit that these arguments are not unfounded and that there is still a long way to go before we can see the technique benefitting patients on a larger scale. “‘Over the past decades a number of patients have received cell transplants. In some, the transplanted cells survive, grow and significant clinical improvements can be seen for many years after the transplant. Yet, in others, the therapy not only fails, but the patient develops side effects” explained Gesine Paul, underlining the complexity inherent in taking cell transplants from the lab to the clinic.
After admitting that the field of cell therapy has plenty of obstacles yet to pass, Dr Paul instilled some new hope in the audience. A wide-ranging, multinational research program – TRANSEURO – is now aiming to develop a best practice for cell therapy. Being part of the Lund TRANSEURO team, Gesine Paul was clearly hopeful that the ongoing study, already performing multicenter clinical trials, will help push the field ahead to a new phase of cell therapy trials in Parkinson’s disease.
As the afternoon turned to evening and the Swedish autumn sun gave way outside the tall windows of the Pufendorf Institute all three scientists took the stage for the final debate. The stage was shared with the three representatives from the Parkinson Movement - Jon Stamford, Sara Riggare and Paul de Ross – and there was no shortage of subject matter as the six of them began touching on the topics of the day.
The lively debate ended on a surprising note as the MultiPark scientists were put on the spot by an unexpected question from a web visitor. Paul de Roos read the question; “If you rubbed a bottle and a genie appeared, what PD-related question would you ask him?”. Patrik Brundin hesitated before deciding upon the question “at what specific event does Parkinson’s disease actually start?”. Gesine Paul took it one step further by suggesting the question “What is the perfect therapy for Parkinson’s?”, admitting that the answer to that question would put her and her colleagues effectively out of a job.
Text: Jens Persson
Page Manager: Jens Persson
Last modified: 2011-11-16
