From the link you gave, Mike, I went to a few other DEFRA sites. The link below was quite interesting. This is a selected quote taken from the page which was last updated Oct 25/05.
It is totally ignoring the work done by Brown, et al. which demonstrates that the healthy prion protein's job IS to balance copper (copper homeostasis) in the brain, and provide copper for anti-oxidant enzymes, of which the prion protein has also been demonstrated to be.
It is also totally ignoring the environmental metals factor which was identified by Mark Purdey, researched by others like Brown, Ragnosdottir, Chalet, Wong, etc. etc.....
There is no mention of the environmental factors which influence the development of TSEs under this "Causal" reference. While some of the work which is out now, may not have been published at the end of October 2005; the government was certainly aware of it. (FATEPRIDE)
What do you do when the government propaganda is so biased? What can we do, when they ignore the research which is, by far, more plausible than the "infectious protein" hypothesis.
When the UK government makes such statements as "
not.. all novel hypothesis will be tested..." everyone should be screaming "foul". If they were as unbiased as they try to say they are, then they would pay for the testing of other novel hypothesis. Instead, they hide behind the lies which they have perpitrated in order to prevent liability against their forced use of the copper chelator "Phosmet" in their government mandated warble eradication program. Not to mention, the contamination of the environment with metals, and radio-active contaminants from various industries.
http://www.defra.gov.uk/animalh/bse/science-research/pathog.html
Causative agents of TSEs
There is still considerable scientific uncertainty about the precise nature of the causative agents of TSEs. The prion protein PrP is a normal membrane-associated protein that is found most commonly in the central nervous system and is very important in the development of TSEs. Modified forms of this protein are associated with infectivity and also accumulate in the brain in the diseased state. The function of the unmodified prion has not yet definitively established.
Put simply, the prion hypothesis says that infectivity is caused by a structurally-modified form of the PrP that promotes conversion of other PrP molecules into the same form. These then accumulate to interfere with the function of nerve cells. However, whether the prion (the PrP protein alone, with no associated nucleic acid) is the cause of BSE is not certain.
Other theories suggest that the causative agent might be a "virino"; an infectious pathogen containing a core of nucleic acid associated with host derived cellular proteins, similar to a small virus. Alternatively, some scientists have argued that a filamentous virus is the cause of TSE.
The prion hypothesis may be the most popular at present, but a number of scientists find difficulties with it, primarily as it contradicts the scientific orthodoxy that the inheritance of a trait, such as disease, must be associated with nucleic acid. MAFF holds no particular position with respect to the nature of the agent as all hypotheses currently remain unproven. This does not, however, mean that all novel hypotheses will be tested by research as most can be tested for a fit with current scientific knowledge about BSE.
This scientific uncertainty over the nature of the causative agent does not, however, affect the validity of the steps taken to control the disease and protect human health. The basic tenets on which the controls were based, namely, that the infective agent is transmitted through contaminated feed and detected only in certain tissues, even in clinically affected animals, apply, whatever the actual form of the agent.
(Page last modified: 25 October, 2005)