Hi Kathy,

I'd love to see a citation for that if you don't mind. It is new to me.

Your warning about relying on abstracts alone is well-taken. I do not understand the abstract you cite from the December 2001 issue of the Journal of Inorganic Biochemistry as seriously disputing the feedborne transmission theory.

Perhaps you would be kind enough to explain exactly what they mean by "somewhat purified"?

In any event, I am not aware of any convincing explanation for the drop in incidence of BSE in the UK following the feed ban, apart from ruminant MBM in feed being the means of transmission. After all, like it or not the UK was and is the biggest BSE experiment in the world. If a model doesn't fit the UK experience on a macro level, then please forgive me if I am not convinced by what any one lab may or may not be able to demonstrate. Reproducibility and peer review is the backbone of good science. Remember cold fusion?

Are you aware of any other epidemiological studies that support an alternate theory of transmission?

I have no dispute with toxicity of metals. Metals may indeed be a co-factor in BSE particularly given that the normal version of the BSE prion binds copper. You may want to have a look at this interesting paper I came across that fits in well with what I take to be the actual conclusion from your 2001 abstract "It is suggested that PrP(C) is a normal Cu-dependent cuproglycoprotein of unknown function that may have a role in facilitating normal nitrogen monoxide- or carbon monoxide-mediated biochemistry."

 http://www.blackwell-synergy.com/doi/pdf/10.1111/j.1471-4159.2006.03906.x

Semi-fascinating idea that the normal version of the BSE prion protects against copper toxicity. What happens when the normal version of the prion is converted to the BSE version (PrP(C) to PrP(Sc))? If the protection against copper toxicity is lost then the symptoms of the disease might look like (and actually be) copper poisoning, don't you think?