- Parkinson's Disease
Advances have relied on human study
For more information, see the longer article here.
Despite claims to the contrary, there is no animal model of Parkinson’s Disease (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 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.
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.
Jay Schneider, one such experimenter who uses animals, 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.” [Greek & Greek ‘Specious Science’, Continuum 2000]
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.” [Kau & Creese in Emerich, Dean and Sanberg (Eds) ‘Central Nervous System Diseases: Innovative Animal Models from Lab to Clinic, Humana Press 2000] 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.
The human and macaque brains - same scale. The size, complexity and functional areas show significant differences, yet macaques remain a favourite animal for brain research.
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. They found that 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.”[ Current Opinion in Neurology 1996;9:303-7]
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 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.”[ Science 2001;291:567-9]
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.[ Science 2001;291:567-9. Parkinsonism and Related Disorders, March 2000]
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 these autopsy studies were seven presentations of either the first complete description of a newly recognized human disorder, or one of the first complete descriptions of an uncommon human neurologic disease.”[ Hill, R. B. and Anderson, R. E. The Autopsy - Medical Practice and Public Policy, Butterworth 1988]
Before the Hornykiewicz discovery, surgery was used to control PD by removing both thalami. The thalamus is a two part brain section. This had limited success, but it was in attempting these that a more striking method was discovered.
Deep Brain Stimulation
To make surgery more accurate, high-frequency electrodes were used to increase activity in neurons to aid the thalamotomy. By chance, a doctor at Grenoble University Hospital in France used the wrong frequency when doing this. Dr Bernabid found that the lower frequency calmed the neurons, and tried applying them to other parts of the brain. Reasoning that this may stop symptoms altogether, he tried to do so, and was successful.
He soon was presented with a patient on whom he couldn’t perform a thalamotomy, so tried implanting the electrodes permanently. It was successful, and led to more research, and the eventual approval of the technique around the world.[ New Scientist vol 183 issue 2457 - 24July2004, page 40]
Bernabid’s discovery was a victory for surgical technique, human study, and observation. It owes nothing to animal experiments. This same technique is the one used by an outspoken supporter of the Oxford University animal lab, and media attention has been drawn to this and a PD patient who uses DBS, as if this was evidence in support of animal testing. We can be absolutely clear that this technique has nothing to do with animal experiments, and everything to do with technology, clinical medicine and observation. Deep Brain Stimulation was not discovered by experimenting on animals.
Technology offers exciting opportunities for research into the brain. See Superior Methods for more details of what it possible in the modern laboratory.
Edit: Parkinson's Disease and the associated cell damage can now be observed in cell culture. Read more here.
Other illnesses affecting the brain
Human illness cannot be researched by using animals. The evidence that proves this played a major part of the decision not to build a similar lab in Girton, attached to Cambridge University. The evidence was written by a doctor and can be viewed by going to: http://www.vivisection-absurd.org.uk/xprimate.html and selecting ‘part 2’.
Some of the other illnesses of the brain are also claimed to be advanced through animal study, but as with PD, progress has only been possible through human study.
MS is caused by the immune system attacking itself, and the cause is not yet known.
Animal models have misled experimenters about how MS progresses and have symptoms and patterns of damage to the brain that are not at all in line with human experience. They have also failed to provide treatments of value.
“Time after time, researchers have discovered new ways to cure laboratory rats of experimental induced encephalomyelitis, the murine model of MS, only to face obstacles in bringing the treatment to humans.”
Treatments developed on animals include Tumor necrosis factor (which has the opposite effect in humans) , Copaxone (which came with numerous side effects), and injected immunoglobins, which were no more effective than placebos . Peptide ligand formulas trials were abandoned as patients nearly died.
Most research into MS has been based on clinical research and culture work using T-cell lines and cells taken from individual patients.
Dr Alois Alzheimer first identified AD using microscopes and autopsy. The lack of mental function is caused by protein becoming uncontrolled and forming protein deposits in the brain now known as neurofibrillary tangles. The particular protein involved (tau) was identified in mice, but altering the mouse’s tau did not even cause any symptoms similar to AD, despite enormous efforts and resources.
The first major breakthrough was the discovery that AD patients lacked acetylcholine, which helps neurons communicate. This was discovered through autopsy.
Animal models have proved frustrating and unproductive:
“The full spectrums of the biochemical and pathological abnormailities characterized by AD have not been found to occur spontaneously in any animal species other than human…”
Another explains: “There is no good animal model for the disease process characterized by a loss of cognitive functions and memory decline.”
While human studies have enabled advances, especially in the knowledge of the genetic implications of AD, a medical journal editorial criticising animal models points out that the first discovered characteristic of AD is not present in animal models:
“More problematically, these animals do not develop neurofibrillary tangles or show significant neurodegeration.”
In a speech at the International Symposium of April 25 1987, Zurich, Dr Med. Bernhard Rambeck, Director of the Biochemistry Department of the Society for Epilepsy Research in Bielefield-Bethel, West Germany stated:
“As a scientist, I am of the opinion that animal experiments bring no progress in the diagnosis and therapy of epilepsies. I have a well-founded suspicion that similar facts apply in other areas of medicine.”
The first accurate description of epilepsy was by John Hughlings Jackson. Long before electroencephalograms (EEGs) he correctly described the illness as one caused by abnormal electrical discharges in the brain. This was based on observing patients, although now, MRIs can show which part of the brain is causing the seizures and how the illness is progressing.
Progress has enabled types of epilepsy to be identified:
“The detailed models for focal interictal discharges arose largely from experiments on brain slices in vitro [studied after death], combined with computer simulations.” 
An evaluation of modern epilepsy research by vivisection supporters recently identified the most important methods as:
•Brain imaging methods, especially MRI
•Surgical technique and the ability to detect opportunities for surgery
Animal experiments were not mentioned.
Attempts to cause an animal model by inducing birth defects in animals were based on the discovery that substance abuse in humans is linked to epilepsy. It didn’t work.
The discovery of treatments has been mainly due to discovering the effects medicines have had on epilepsy when intended for another condition. “Overwhelmingly, discovery of the old and a number of the new AEDs [antiepileptic drugs] came from serendipity [chance].”
The idea that animal models would enable this is dismissed:
“In other words, a potent new drug against NMDLA ot NMDA-induces seizures [animal models of epilepsy] is not necessarily a useful drug for therapy of drug-resistant epilepsy (in humans) as demonstrated by the disappointing data from clinical studies with NMDA antagonists in patients with refractory epilepsy.”
Although dogs can naturally develop epilepsy, comparing human and dog patients is not viable due to the way the drugs are handled by the bodies. Vigabatrin treats epileptic dogs, but when given to human was related to severe vision damage and has led to large court cases.
The claim by animal experimenters that their practice has been invaluable is false. It is also a claim which other researchers feel is detrimental to the advancement of science. Concern about the preoccupation with animal research is becoming more prevalent.
The evidence that animal experiments are bad science and hamper the progress of human medicine is overwhelming and more doctors are coming to the conclusion that vivisection is a deeply flawed scientific practice. Vivisectors want to continue with animal experiments not because it’s the best form of research but because it keeps them in their chosen career. It’s vitally important that for those people suffering from terrible illnesses, that the fraud is stopped now.
Unsurprisingly, animal experiments are seen as a poor method of studying human illness and are rapidly becoming less respected. As two pathologists explain:
“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 these autopsy studies were seven presentations of either the first complete description of a newly recognized human disorder, or one of the first complete descriptions of an uncommon human neurologic disease.” 
See the following websites for more information:
www.curedisease.net - Doctors’ group Europeans from Medical Progress
www.vivisection-absurd.org.uk - Masses of evidence covering news, historical records and other evidence.
http://aerzte-gegen-tierversuche.tierrechte.de/i.php4?Lang=en - European doctors’ group – in English
Other illnesses have been the subject of high profile claims in favour of animal testing. Read the reality here.
1 Greek & Greek ‘Specious Science’, Continuum 2000 back
2 Kau & Creese in Emerich, Dean and Sanberg (Eds) ‘Central Nervous System Diseases: Innovative Animal Models from Lab to Clinic, Humana Press 2000 back
3 Nuc Med Biol 1998;25:721-8 back
4 Current Opinion in Neurology 1996;9:303-7 back
5 Science 2001;291:567-9 back
6 Science 2001;291:567-9. Parkinsonism and Related Disorders, March 2000 back
7 Hill, R. B. and Anderson, R. E. The Autopsy - Medical Practice and Public Policy, Butterworth 1988 back
8 Journal of the Neurological Sciences 1998;9:71-90 back
9 Reuters health, October 18th 2000 back
10 New Scientist vol 183 issue 2457 - 24July2004, page 40 back
11 Reymond in Comparative Primate Biology (vol 4): Neurosciences, by H. S Steklis and J. Erwin, 1988, p605. Dr Hepp-Reymond in Comparative Primate Biology (vol 4): Neurosciences, ed by H. S. Steklis and J. Erwin, 1988 p605. back
12 Neurology 1981;31:600-02 back
13 Jean Martin Charcot, Quoted in ‘Clinical Medical Discoveries’, Bayly, B, NAVS London, 1961, p27 back
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24 N Engl J Medicine 1999;340:1970-9 back
25 Mconner and Tuszynski in Emerich, DG, Dean III, DL & Sanberg, PR (Eds) Central Nervous System Diseases: Innovative Animal Models from Lab to Clinic Humana Press 2000, p66 back
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27 Nature 1999;400:116/17 back
28 Current Opinions in Neurology 1998;11:123-127 back
29 Dr Med. Bernhard Rambeck, Director of the Biochemistry Department of the Society for Epilepsy Research in Bielefield-Bethel, West Germany. Speech at the International Symposium of April 25 1987, Zurich back
30 Epilepsia 1999;40:811-21 back
31 Sperber EF et al ch8 p161-169 in Jaspers Basic Mechanisms of Epilepsies, Third Edition: Advances in Neurology Vol 79 edited by AV Delgade-Escuetta, WA Wilson, RW Olsen & RJ Porter. Lippincott, Williams and Wilkins 1999 back
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34 J Neurol Neurosurg Psychiatry 1999;67:707-708 &716-722. Progress in Neurobiology 1997;53:239-58 back
35 Hill, R. B. and Anderson, R. E. The Autopsy - Medical Practice and Public Policy, Butterworth 1988 back
Other illnesses have been the subject of high profile claims in favour of animal testing. Read the reality here.