Discovery brings BSE and CJD treatments a step closer
20 November 2009
Researchers at the University of Leeds found that the presence of a protein called glypican-1 leads to a rise in the number of abnormal prions, the cause of bovine spongiform encephalopathy (BSE), which affects cattle.
When levels of glypican-1 were reduced in infected cells, they found that the levels of the abnormal prion were also reduced.
According to Professor Nigel Hooper, who led the research, the findings have implications for the treatment of both BSE and vCJD.
"Now that we know the identity of one of the key molecules in the disease process, we may in the future be able to design drugs that target this."
BSE is caused by an infectious and abnormal form of the prion protein, which is present on cells within the nervous system. But what causes the prions to become abnormal has been unclear.
The researchers suggest that glypican-1 acts as a scaffold bringing normal and abnormal forms of the prion protein together. This contact causes normal prions to mutate into the infectious form.
They now hope to conduct further studies to investigate their hypothesis.
Image: Cows. Credit: rightee on Flickr
Reference
Taylor DR et al. Glypican-1 mediates both prion protein lipid raft association and disease isoform formation. PLoS Pathog 2009 [Epub ahead of print].