24th April marks World Day for Laboratory Animals. Recognised by the United Nations as a day of international commemoration. It is a time to reflect upon the pain and suffering caused to millions of animals all in the name of a fraudulent scientific practice - a practice that is not only is so cruel to the animals so horribly abused and killed by vivisectors, but a practice that so cruelly gives false hope to those with illness and disease.
It is therefore fitting that on this day the lies of Tipu Aziz are once again exposed for the world to see. The following article was written by scientist Dr Claude Reiss who specialises in research work into Alzheimer's, HIV and Parkinson's disease using non animal methods. The article highlights the lies of Tipu Aziz and illustrates just what lengths the man is prepared to go to in order to court fame and media attention.
Three questions will be looked at in this article and deals with the 3 main lies that Tipu Aziz often attemtps to propogate:
(1) What is Prof. Aziz’s contribution to deep brain stimulation (DBS) and has work in MPTP- treated monkeys been relevant for DBS? (2) Are more monkey studies aimed at Parkinson disease (PD) needed? (3) Is spending money in DBS tinkering in monkey brains a priority?
(1). I do not question the skills of Prof Aziz as a neurosurgeon practicing DBS. His claim to be the discoverer of DBS is however at odds with the fact that DBS was discovered by chance by a team lead by LA Benabid in Grenoble (France). They published their observations in:
Appl Neurophysiol. 1987;50(1-6):344-6
“Combined (thalamotomy and stimulation) stereotactic surgery of the VIM thalamic nucleus for bilateral Parkinson disease.
Benabid AL, Pollak P, Louveau A, Henry S, de Rougemont J.
Department of Neurosurgery, Grenoble University, La Tronche, France.
According to this paper:
Stereotactic thalamotomy of the thalamic nucleus ventralis intermedius (VIM) is routinely used for movement disorders. During this procedure, it has been observed that high-frequency (100 Hz) stimulation of VIM was able to stop the extrapyramidal tremor. In patients with bilateral tremor of extrapyramidal origin, who were resistant to drug therapy, the therapeutic protocol associated (1) a radiofrequency VIM thalamotomy for the most disabled side, and (2) a continuous VIM stimulation for the other side using stereotactically implanted electrodes, connected to subcutaneous stimulators. VIM thalamotomy relieved the tremor in all operated cases. Side effects were mild and regressive. VIM stimulation strongly decreased the tremor but failed to suppress it as completely as thalamotomy did. This was due in part to the fact that programmable stimulator frequency rate is limited to 130 Hz, while it appeared that the optimal stimulation frequency was 200 Hz. This therapeutic protocol appears to be of interest for patients with bilateral extrapyramidal movement disorders.
This paper appeared in 1987, several years before papers bearing the name of Tipu Aziz were published, according to PubMed records. Whether Prof Aziz was unaware of this paper (and a series of others dealing with the same topic, published before 1992) or decided to investigate DBS in monkeys despite that he knew of its success in humans, is an open question. The Grenoble team’s work demonstrated that DBS allowed to access and temporary minimize or even suppress a series of debilitating brain disorders including PD. It opened the door for the selection of more efficient local brain targets. It is true that the application of DBS to the subthalamic nucleus, which is of improved efficient on tremor, rigidity and bradykinesia compared to VIM stimulation and is now widely applied, has been suggested by experiments in MPTP monkeys (inactivation of the subthalamic nucleus as treatment of PD was suggested already in 1990 by Bergman et al Science 249 pp 1436-8). As the application of DBS to PD sufferers was rapidly promoted following the discovery of the Benabid team, there is no doubt that the benefit of subthalamic nucleus stimulation would have been have been found without monkey experiments.
Prof. Aziz further claims that work on DBS in monkeys was critical for preparing surgery in human brains. First, according to PubMed records, Benabid’s team studied DBS exclusively in human patients, not in monkeys. Indeed, they content that “criteria for DBS success are correct patient selection and precise electrode placement in an area bestowed with critical functions”, like speech. During DBS surgery, which may last for up to 10 hours, the patient is awake and invited to speak, to secure that no damage is made to relevant brain regions. Since architecture and size of monkey brains are vastly different from those of the human brain, any “transfer” of surgical field knowledge from animals to humans is a questionnable and risky exercice. The human brain architecture and functional organisation are much better documented and detailed than those of monkey brains, thanks in particular to non-invasive imaging techniques (which are permanently used during DBS surgery). Training surgery in monkey brains is therefore of no interest for practice in humans.
(2) Thousands of PD research programmes involving monkeys were carried out worldwide over the past 150 years, none succeeded, as there is still no cure (l-dopa and DBS are temporary paliatives only). This is no surprise, since, as far as we know, no monkey develops PD in the wild. More fundamentally, there is a rigorous proof * that no species is a reliable biological model for any other species, whatever close these species may be in evolutionary terms (e.g. human and chimpanzee). This is specially the true for neurological cases. Since it is therefore impossible to have a monkey model relevant for human PD, and given the thousands of documented failures when attempting to overcome this impossibility, is it necessary to add another attempt?
(3) Therefore, research aiming at PD prevention, early diagnosis and therapies at least halting disease progression has absolute priority over DBS tinkering in monkeys. The molecular basis of PD are known, this condition is linked to protein misconformation, just like other so-called conformational diseases (Alzheimer, diabetes type II, “mad cow” disease, Friedreich attaxia and a collection of other severe conditions). We begin to understand the reasons for misconformation of proteins, my team is working towards an sensitive detection of its occurrence (hence early diagnosis of the disease) and a possible immunotherpy to stop its further development. Our research is hampered by lack of funding. Research money is limited, the part taken by projects involving animal models, which are from the onset guarantied to fail, is missing for projects having at least a reasonable chance to contribute progress.
* the biological activity of an individual, including its response in a test, is fully dependent on its precise genetic outfit (chromosomes). A species is defined by its reproductive isolation (its members cannot cross productively with members from any other species), because the genetic outfit of the members of this species is unique (its chromosomes cannot complement those of another species). Therefore, the biological activities of individuals from two species are different, including their reponse in a test.