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Parkinson's disease tests on monkeys 'the BUAV responds

The BUAV has expressed its profound concerns and reservations regarding the highly invasive experiments involving monkeys that were announced today using Oxford Biomedica's Parkinson's disease drug ProSavin.1 These concerns include:

'The monkey "model" for Parkinson's disease has significant differences to human Parkinson's disease, which seriously affect its clinical relevance.2 Artificially producing Parkinson's-like signs in monkeys by injecting their brains with a toxin does not faithfully model human Parkinson's disease.

'The ProSavin intervention only addresses one aspect of the many facets of Parkinson's disease 'dopamine loss. Elucidation of Parkinson's pathology and the progress of the disease has been and will continue to be via the use of superior human-specific scientific methods, such as brain-imaging techniques, use of post-mortem brain tissue from patients, human genetic studies and population studies.3 People knowledgeable in the field recognise this:

"Alzheimer's, Parkinson's and other neurodegenerative diseases occur in humans and it is in human tissue that we will find the answers to these diseases" - Dr. John Xuereb, Director of the Cambridge Brain Bank and Wolfson Brain Imaging Centre. BBC Radio Cambridge, 7th February 2002.

'The monkey can neither be considered to usefully augment the existing human data, nor to increase the probability that ProSavin will be successful in larger and more comprehensive human trials and/or in the clinic. This is due to significant and intractable species differences between humans and monkeys. Such differences mean that 'while occasional correlations do occur - results from animal models are not predictive of human response. Only clinical trials can provide reliable and relevant information regarding the drug's safety and efficacy in humans4 'and these are already being conducted. Notably, there are many superior scientific approaches to testing drugs prior to human trials that do not use animals. When used in concert, these tests 'such as microdosing, toxicogenomics, computer modelling and batteries of human cell and tissue assays 'predict more efficiently the likelihood of success or failure in patients.5

'The clinical results are preliminary: many drugs appear promising in early clinical trials yet go on to fail in later-stage investigations (such as Cephalon's CEP-1347).6

The BUAV agrees that it is important to find a cure for human Parkinson's disease and to alleviate the suffering it causes. However, the monkey experiments reported in the ProSavin article were cruel, unnecessary, irrelevant and not predictive for humans. Despite decades of research, much of it using monkey "models" of Parkinson's disease, there is still neither a cure nor any treatment that halts the progress of the disease or is effective against its symptoms in the long term.

Until more researchers join the ranks of forward-thinking scientists who utilise human tissue and perform ethical human studies, Parkinson's research will continue to stall and throw up disappointments in the form of new drugs and interventions that "worked" in animals but do not in people.

Citations:

1. http://www.reuters.com/article/scienceNews/idUSTRE59D4DL20091014

2. Hantraye P. Modeling dopamine system dysfunction in experimental animals. Nucl Med Biol. 1998 Nov;25(8):721-8. Bailey J. Non-Human Primates in Medical Research and Drug Development: a Critical Review. Biogenic Amines 2005;19(4-6):235-255. Schober A. Classic toxin-induced animal models of Parkinson's disease: 6-OHDA and MPTP. Cell Tissue Res. 2004 Oct;318(1):215-24. Epub 2004 Jul 28.

3. Bruck A et al (2001) Positron emission tomography shows that impaired frontal lobe functioning in Parkinson's disease is related to dopaminergic hypofunction in the caudate nucleus. Neurosci Lett. 311:81-84. Sanai N et al (2004) Unique astrocyte ribbon in adult human brain contains neural stem cells but lacks chain migration. Nature 427: 740-4. Dawson TM and Dawson VL (2003) Molecular pathways of neurodegeneration in Parkinson's Disease. Science 302:819-822. Ascherio A et al. (2006) Pesticide exposure and risk for Parkinson's disease. Annals of Neurology 60: 197-203. Marvanova M et al. (2003). Microarray analysis of nonhuman primates: validation of experimental models in neurological disorders. FASEB J 17, 929-931.

4. Harding, A. (2004). More compounds failing phase I. FDA chief warns that high drug attrition rate is pushing up the cost of drug development. The Scientist (6 August).

5. Bailey J, Taylor K. The SCHER report on non-human primate research - biased and deeply flawed. Altern Lab Anim. 2009 Sep;37(4):427-35.

6. http://www.pdpipeline.org/advocacy/cephalon_halts_cep1347.htm

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