Parkinson's - The Truth

Parkinson’s disease (PD) is a terrible illness which causes enormous human suffering. Supporters of the new Oxford University animal lab claim that experimenting on animals will enable advances in treating PD. We have always expected animal experimenters to defend the proposed lab; their careers, reputation and future income depend on projects such as this continuing. Unfortunately for them, neither medical history nor science supports their claims.

The reality is that there is no animal model of PD, and all past advances in treating it have been made through human study. In future, animals are of even less value as a research method – for two reasons. One is that we are studying PD in greater details, and the vague similarities between animal and human biology will be less relevant. The other is the emergence of incisive technology which enables the study of the human PD patient at levels we would hardly have believed possible years ago.

The claim that animals have or will be helpful in tackling the disease is hollow. Our opportunity to prove this is our opportunity to take away the assertion that the Oxford animal lab has any place at all in modern medical research. This means that we all need to know why PD research fails in animals and how advances really have and will be made.

We will therefore be looking at 5 specific subjects in order to highlight the fraudulent arguments being made by the pro vivisectionists:

• The vagueness of the animal model
• Understanding and treating PD
• Deep Brain Stimulation
• Technology in the modern laboratory
• Other illnesses affecting the brain

The vagueness of the animal model

The cause of PD is specific – it’s caused by degeneration of a specific part of the brain. Animals don’t get it, and the best animal experimenters have managed to do is recreate some of the symptoms.

Wild Tufted Ear Marmoset. Monkeys like this one are used in Parkinson's research The favourite way of doing this is to apply MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) to the brains of animals. MPTP is a by-product of synthetic heroin. The problem with this method is that it doesn’t cause PD – it just causes illness which shares some of the symptoms. Even the animal experimenters who practice it – usually experts in blowing their own trumpets and exaggerating the value of their work – criticise it and they don’t claim animals with it have Parkinson’s.

Jay Schneider, one such experimenter, calls it ‘parkinsonism’, and writes: “Some monkeys had cognitive deficits and no motor deficits. Other monkeys had full parkinsonism that was produced after short-term high dose MPTP exposure, and some monkeys had full parkinsonism after long-term low-dose MPTP exposure.”[1]

“…it is essential to understand that animal models only represent an imperfect replica of human disorders, and this is so for several reasons. First, animal models are generally developed in beings (rodents, non-human primates) that are subjects with behavioural repertoires and anatomical characteristics very different from humans. These species differences are known to play a critical role in the clinical expression as well as in the cellular specificity of the lesions. Second, in addition to these species differences, the time source evolution of the nerve cell generation, which normally evolves over several years in neurodegenerative diseases in humans is for practical reasons being replaced over a much shorter period of time in animal models. ”[3]

Is this haphazard set of symptoms supposed to be a scientific model? As if to add to the uselessness of the model, the animal model recovers gradually – unlike the chronically afflicted human patients. An expert explains that: “The best model of PD to date, is the…(MPTP)-lesioned marmoset….unlike human PD, which is progressive, the neurotoxic damage produced by MPTP is reversible.” [2] The suggestion that gradually recovering monkeys with a condition that causes variable symptoms can be used to study the disease is clearly ludicrous.

A further problem which would render animals useless as a method if they weren’t already is that communication between animals and human is so limited. Animals can’t explain their symptoms, emotions, difficulties in motor functions or what affects them in everyday life.

In summary, the animal model is a failure because:

Animals don’t get PD

The ‘best’ animal model recovers and has some similarities of symptoms – not PD

Animals can’t communicate well with humans, and have different behaviour from humans

The illness is induced quickly – unlike the slow degeneration in humans.

Given that animals are a failed method, how has progress been possible against PD? As for the overwhelming majority of illnesses, progress has been due to a combination of study of patients, autopsy, the use of technology and a helping of luck.

Understanding and treating PD

PD was never really understood until 1960. An Austrian team lead by Oleh Hornykiewicz performed autopsies on human PD patients at the University of Vienna. The knowledge at this point – established by autopsy - was that this very specific, human illness, was caused by a very specific part of the human brain degenerating. The substantia nigra, part of the brain found in the basal ganglia was badly affected. This was never likely to be uncovered in animals, who don’t have a comparable basal ganglion. As an expert explains, animal models “do not reflect the complexities of the human basal ganglion.”[4]

The Austrian team discovered that the nigostriatial pathway had degenerated and had very little dopamine. Dopamine regulates movement and emotion, and normally carries most of the nerve signal.

This made perfect sense as PD does affect movement and emotion, and led to tests on brain tissue from PD patients, which confirmed the dopamine deficiency. They went on to discover that nerves containing dopamine die, leaving a deficiency of dopamine. They soon gave patients treatment intended to lead to dopamine production, which caused immediate benefits. As well as revolutionising PD treatment, this enabled better research into other neurological illnesses including epilepsy and schizophrenia. As one expert put it, Hornykiewicz had “fundamentally changed how neuropharmacology is practiced.”[5]

Hornykiewicz was never awarded the Nobel Prize for this work, although it was awarded to a team who had followed on from the work pioneered by the Austrians. The award attracted disapproval: 250 neurologists criticised the decision and the decision not to reward Hornykiewicz.[6]

This massive discovery is only a step on the way to finding a cure for this terrible disease. The fact that the substantia nigra dies is a symptom, not the cause of the disease, and further knowledge of why it dies needs to be uncovered. For this reason why need more studies into human patients on a detailed level studying the interactions between the substantia nigra and the rest of the body. Autopsies are now possible on a highly detailed level thanks to improvements in microscope technology, and arguably provide the most valuable of any single method in studying nerological illness.

Two pathologists wrote “In recent years, participants in meetings of the American Association of Neuropathologists have heard criticism about the increasing use of animal models to study human neurologic disease…. A strong cadre of diagnostic and research neuropathologists believe that only human material can provide relevant answers to many problems about human central nervous system disease. In fact, examination of the data bears out this contention. Of the 185 abstracts presented at the 1985 meeting of the American Association of Neuropathologists, 115 (62%) were presentations of human neuropathology, and an astounding 81 (43%) were based on investigations of human brains at autopsy. Among the