• Home
• About us
• Take action
• Campaigns
• Media centre
• Publications
• Store

Issues

• About vivisection

• Alternatives
• Animal experiments: the facts
• Ask NAVS
• Investigations
• Legislation

• Animal rescues
• Research
  without animals
• Animal Defenders International
• My Mate’s a Primate

• Jobs at NAVS

• Translation

3. The Scientific Steering Committee’s five examples of diseases of concern

13 July 2007

(e) Immune-based diseases

SSC: “Non-human primate models…are needed for the development and evaluation of new immunomodulatory/immunosuppressive therapies”.

ADI Response, Multiple Sclerosis:

• The key laboratory animal model of multiple sclerosis (MS) is called experimental allergic encephalomyelitis (EAE); a condition caused by the injection of toxic substances which causes the immune system to attack the nervous system.
• However, it differs in that it either kills the animal or leaves it with permanent disability; it does not come and go like MS59.
• Not a single human has been cured using the EAE approach, which has been used to test virtually all MS treatments59. EAE is a laboratory-created tool rather than a spontaneous disease with a complex development, and therefore relieving the symptoms of EAE is not predictive of relieving MS. Its various models also make it difficult to use for drug screening60.
• It has been suggested that the EAE model is misleading and that the best way forward without the EAE model restraining MS research, would be to look at the patients themselves61. Measuring relapse rate, disability and MRI scanning of lesions in the brain enables the assessment of disease activity in MS62, which is used to determine individual therapies, necessary because of the diversity of the disease in individual patients63.

ADI Response, Diabetes:

• Unlike many genetic disorders that are due to a single defective gene, with diabetes several genes seem to be responsible. Environmental influences also play a part64. Clinical research has shown that juvenile onset diabetes occurs more commonly in the autumn, when viral infections are more prevalent65. There are huge disparities in the prevalence of diabetes in different human populations around the world. The disease is increasing in children under 5 in Finland and the UK, which it has been said points to “Major aetiological factors early in life, such as viral infections and nutritional factors”66.
• In NHPs diabetes-like symptoms are induced using chemicals because “spontaneous development of type 1 diabetes mellitus has not been reported in non-human primates”. The model has its limitations including the “absence of spontaneous immune-mediated beta cell loss”67.
• In 1977 an eminent diabetes clinician said of animal models of diabetes “…they do not help us in our understanding of the genetics of human diabetes”68. Twenty years later, other researchers confirmed that this remained true, “The most reliable way of elucidating the cause of a disease is to study it in the animal species and in the environment in which it naturally occurs”69.

SSC: “There is an increasing need of non-human primates as models for CNS biology and disease”.

ADI Response, Central Nervous System (CNS) diseases (Alzheimer’s, Parkinson’s, Multiple Sclerosis, etc):

• There are enormous differences in monkey and human brains. Researchers at the Institute of Neurology in London recently blamed “remarkable species differences” for the failure to apply primate findings to human brains70.
• The chimpanzee brain is about one quarter the size of the human brain and the macaque brain is around one quarter the size of the chimpanzee brain. Comparisons between these brains are limited by the greater complexity of the human brain, due to its larger size, and exemplified by its unique capacity for language24.
• Often, areas in the brain that appear to have a function in monkeys do not have the same role in humans25.
• Researchers at two prestigious institutions, the Salk Institute and the University of California wrote: “What is known about the neuroanatomy of the human brain? Do we have a human cortical map corresponding to that for the macaque? And what does the human equivalent of the connectional map look like? The shameful answer is that we do not have such detailed maps because, for obvious reasons, most of the experimental methods used on the macaque brain cannot be used on humans. For other cortical regions, such as the language areas, we cannot use the macaque brain even as a rough guide as it probably lacks comparable regions”71.

SSC: “The close genetic, immunological and virological relation with humans makes non-human primates an excellent model of this disease [MS]”.

ADI: A recent paper on animal models of MS reported the withdrawal of a drug after one patient died and another became seriously ill. It commented “efficacy tests in animal models do not account for the clinical situation”72. The drug had been tested on primates, but no similar condition was observed; the authors stated “Spontaneous cases of MS-like disease rarely occur in common laboratory species ... the disadvantage of these experimental MS models is that none of them reproduces the complete clinical and pathological spectrum of the disease”73.

Send this page to a friend