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2. The Scientific Steering Committee position

Posted: 13 July 2007

“[SSC] ...considers that non-human primates are required in biomedical research for the following reasons:

1. to ensure safety. Many new vaccines or biologicals must be assessed for specificity and safety in a “near-human” immune system before they enter the clinic.

2. to determine the efficacy of non-human primate models for infections for which no other suitable animal models exist. These so-called “proof of principle” studies are critical in catalysing interest and development capital for development and clinical trials.

ADI Response – safety and efficacy/species differences:

There have been no systematic reviews of animal research and testing to confirm whether this methodology is providing the assurances of safety that the public expects:

• The Toxicology Working Group of the UK Parliament’s House of Lords Select Committee on Animals in Scientific Procedures reported in 2002, saying “the formulaic use of two species in safety testing is not a scientifically justifiable practice, but rather an acknowledgement of the problem of species differences in extrapolating the results of animal tests to predict effects in humans”, and, “the reliability and relevance of all existing animal tests should be reviewed as a matter of urgency”19.
• A study carried out in 2005 demonstrated that many common drugs and household chemicals have been certified as safe for humans on the basis of animal tests that are accurate, on average, just over half the time20.

Primate experiments cannot guarantee safety, and can be dangerously misleading:

• In 2006, the first human trials of the experimental drug TGN1412 in the UK caused volunteers to suffer serious, and permanent, life-threatening damage. Prior to human trials, the drug was tested on monkeys. The monkeys received 500 times the human dose but did not suffer the side effects experienced with the volunteers31. Several studies, specific to TGN1412, have highlighted the crucial differences between the human and simian immune systems21.

The use of NHP is often justified as the ‘only’ way to conduct research into neurological diseases such as Alzheimer’s and Parkinson’s, which are increasing with the ageing population – people are living longer. It is estimated that the number of people with cognitive impairment in England alone, is likely to rise by 66% between 1998 and 203130.

However there is now evidence that both behavioural neuroscience and other neurological experiments on animals are fundamentally flawed due to species differences. For example:

• Human brains have a folded cerebral cortex whereas smaller primates, such as the marmoset, have a smooth cerebral cortex. Not only are there anatomical differences between the two brain types, but evidence suggests that there are functional differences, too22.
• Lower and higher primates differ in a number of structural features in their nervous systems and sense organs. Lower primates’ brains are much smaller in relation to body size than those of the higher primates. The areas which govern the transfer of information between the different brain centres, differ in development between brains of higher and lower primates23.
• Animal models of Alzheimer’s do not develop the characteristic ‘neurofibrillary tangles’ or show significant neuro-degeneration as humans do26.
• The drug MPTP is used on non-human primates to attempt to create a ‘model’ of human Parkinson’s disease. However, Parkinson’s disease is unique to humans27 and slowly progressing, whereas MPTP-induced Parkinsonism is rapid in its course. There are differences in nerve degeneration and the transmission of nerve impulses in naturally occurring human Parkinson’s disease and MPTP induced Parkinson’s disease in animals28. There are major differences at both the behavioural and nerve chemistry levels between different monkey species when given MPTP29.
• Drs Palfreyman, Charles and Blander in ‘Drug Discovery World’ observed: “One of the major challenges facing the drug discovery community is the poor predictability of animal-based strategies . . . many drugs have failed in later stages of development because the animal data were poor predictors of efficacy in the human subject . . . . One of the overriding interests of the pharmaceutical and biotechnologies industry is to create alternative development strategies that are less reliant on poor animal predictor models of human disease...”32.
• It has been noted that the way drugs break down and are excreted are similar in monkeys and humans, but metabolism rates differ markedly33, and the cynomolgus macaque has been referred to as the most misleading laboratory animal model for the study of toxic effects on the human heart34.
• Evidence is mounting that standard lab conditions cause enough stress to affect the physiology of research animals. The concern is that this change in physiology will swamp the effects of experimental perturbutation or drug35.

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