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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.