In a post a couple of weeks ago entitled “End of primate research at the University of Toronto?” Allyson Bennet wrote about the truth behind the spin that primate research has ceased at the University of Toronto (UT), commenting that:
If nothing else, those inclined to dodge should consider that they are deriving benefit from the work of their colleagues at the institutions still willing to assume the risk and responsibility.”
It hasn’t taken very long for other animal rights groups in Canada to pick up on UT’s perceived change of policy, with a Vancouver-based group named STOP UBC Animal Research (STOP) quick to demand that the University of British Columbia (UBC) follow UT’s example.
For more than a year now STOP have been engaged in a high-profile campaign against animal research at UBC, prompting UPC to respond by providing information about the animal research they undertake. One of their main targets has been Professor Doris Doudet, who employs advanced imaging modalities such as positron emission tomography (PET) for the evaluation of functional, neurochemical, and anatomical changes in the brains of animal models of Parkinson’s disease.
In a paper published online last November in the Journal of Cerebral Blood Flow and Metabolism Professor Doudet and her colleagues reported that they had used PET to confirm that abnormal metabolic patterns recently observed in the brains of Parkinson’s disease patients are also found in the brains of monkeys which have been treated with the drug MPTP to kill the dopamine producing neurons in the brain and induce Parkinsonism. This result both confirmed the close similarity between MPTP-induced Parkinsonism and Parkinson’s disease, and provides another useful way in which the effects of candidate therapies for the treatment of Parkinson’s disease can be evaluated in this much-used animal model of Parkinson’s disease.
Unfortunately in the course of the experiment four of the eleven monkeys treated with MPTP developed an unusually severe response, and rather than recovering after the experiment – as is usually the case with monkeys treated with MPTP – they had to be euthanized. The Journal of Cerebral Blood Flow and metabolism paper makes it clear that Prof. Doudet and her team responded quickly and correctly to the unexpected situation to minimize any suffering the animal’s experienced.
Not surprisingly STOP are seeking to make capital out of this event…but this is where animal rights propaganda parts company with the facts.
In a statement to the UBC student newspaper Ubyssey STOP claim that far from being accidental the four monkey deaths were planned:
a 2010 progress report on Doudet’s study indicated four monkeys were to be “sacrificed to neuropathology”—two at the six-month mark after showing mild symptoms of Parkinson’s, and the final two after twelve months.
“Animals should be able to recover from the Parkinsonism that researchers inflict on them,” Birthistle said. “She’s intending to kill them all along, and then they’re talking about it as being unforeseen circumstances.””
So what is this “2010 progress report? Well, another statement by STOP quoted in a Vancouver newspaper explains that they are referring to a study named “L91”.
So what is L91 all about?
It’s not the first time that STOP have complained about study L91, back in January of last year they staged a protest against it. L91 is a project planned by Prof. Doudet to use PET to study the effect of injection of the proteasome-inhibitor Lactacystin on the brain function of four macaques, and a description of the proposed project can be found on page 25 of this TRIUMF publication. Lactacystin injection is a relatively new animal model of Parkinson’s disease, recreating the damage to the proteasomes of the dopamine secreting neurons of the substantia nigra region of the brain observed in Parkinson’s disease patients, and has the potential to become a valuable resource for evaluation new therapies.
So it’s abundantly clear that the proposed study L91 is NOT the same as the study published last November in the The Journal of Cerebral Blood Flow and Metabolism, as the former plans to use lactacystin to induce Parkinsonism while the latter used MPTP. It is equally clear that STOP are well aware that these are not the same study, as they have access to all the relevant documents.
Yet, not only to STOP repeatedly and dishonestly claim that these are the same study, but on the basis of this claim they go on to make false allegations of professional misconduct against Prof. Doudet and demand that UBC suspend her from her duties and carry out a full investigation.
And I’ll bet that they will express surprise and outrage when UBC refuses to comply with their demands!
Before leaving this subject it’s worth addressing the importance of the role of animal research in Parkinson’s disease research, something that we are well aware of thanks to Pro-Test’s own Prof. Tipu Aziz, whose research using the MPTP model of Parkinsonism made major contributions to making deep brain stimulation (DBS) for Parkinson’s disease the success it is today. I’ll value the views of the neuroscience community as a whole – including great neuroscientists such as the physician-scientist Prof. Alim-Louis Benabid, pioneer of DBS for Parkinson’s disease – over those of the few fringe scientists that STOP can scrape together. Prof. Benabid and other genuine experts on Parkinson’s disease recognize that while Parkinsonism models such as the MPTP monkey do not recreate every aspect of Parkinson’s disease they play a vital role alongside clinical research in uncovering the process that cause the disease and its symptoms, and in the development of new therapies for Parkinson’s disease.
As Prof. Benabid wrote in a review in 2004:
The knowledge of the functional changes of basal ganglia activity in the parkinsonian state as it emerged from extensive experimental studies on animal models has provided the theoretical basis for surgical therapy in PD. The 6-hydroxydopamine (6-ODHA) rat model and the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) primate model of PD provided powerful research tools for uncovering the pathophysiology of changes in functional basal ganglia activity in PD. “
and in a review published this year
The specific effect of DBS at high frequency, discovered during a VIM thalamotomy, was extended to the older targets of ablative neurosurgery such as the pallidum, for tremor in Parkinson’s disease (PD), dyskinesias, essential tremor, as well as the internal capsule to treat psychiatric disorders (OCD). A second wave of targets came from basic research (in this instance animal research –PB), enabled by the low morbidity, reversibility, and adaptability of DBS. This was the case for the subthalamic nucleus (STN) which improves the triad of dopaminergic symptoms, and the pedunculopontine nucleus (PPN) for gait disorders in PD. “
As with so many areas on medicine it is the confluence of animal and clinical researhc that is driving advances in the treatment of Parkinson’s disease.
Rather ironically animal rights organizations like STOP and their supporters are very quick to claim that Prof. Benabid’s serendipitous discovery that electrical stimulation of the ventralis intermedius could reduce the tremor associated with Parkinson’s disease demonstrates that research using the MPTP model is unnecessary. They seek to co-opt his stature as a leading neuroscientist while simultaneously ignoring the fact that he not only recognizes the importance of animal models of Parkinson’s disease but himself undertakes studies with the MPTP Monkey model and other animal models of Parkinson’s disease.
So, the question is who you are going to believe, leading neuroscientists like Prof. Doudet and Prof. Benabid, or STOP? Somehow I doubt it will take you long to come to a decision!