National Antivisection Society
Research on TSE
Posted: 13 July 2007
The SSC included research on TSE in its introduction, citing research on these diseases of the brain to justify the use of non-human primates in research:
ADI Response: TSE (spongiform encepalopathy, e.g. scrapie, BSE, CJD):
- Infecting animals may be pointless – some scientists have suggested that the apparent increase in CJD may not be due to BSE infection, but since the BSE crisis doctors have increased their vigilance and are detecting a naturally occurring disease93. Before the BSE crisis, doctors missed nearly two-thirds of all classical CJD cases94, and some said “there is no epidemiological evidence to support a relationship between sporadic CJD and scrapie (or any other animal TSE)”100.
Furthermore, the NHP model is a poor representation of the human disease:
- A study to show the effects of feeding infected brain tissue to macaques resulted in one animal becoming infected, which subsequently died, while another was unaffected. It was concluded that the data did “not provide a definitive minimum infective dose for transmission of cattle BSE to primates”. It was furthermore noted that in order to match the level of infective material given to the macaques, a human being would have to consume 1.5kg of infected brain material95.
Human studies on the other hand, provide better information on the epidemiology and pathogenesis of the disease:
- All vCJD victims have had a particular combination of prion genes – this is present in 38% of the population96.
- It has been stated “Particular combinations of psychiatric and neurological features may allow early diagnosis in an appreciable number of patients”; such signs include numbness, handwriting impairment, “odd sensation” and dizziness. These features cannot be identified in primates, making them a poor model for this research97.
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