HOPES for a treatment for the human form of mad cow disease have been raised by development of antibodies that protect mice against scrapie. But there鈥檚 a catch: the antibodies only work if given before symptoms appear.
So far, 125 people in Britain have died of variant Creutzfeldt-Jakob disease (vCJD), and a further seven are suspected of having the disease. One is being given pentosan polysulphate, a drug normally used to treat cystitis, but no results have been announced.
The antibodies, developed by a team led by Simon Hawke of Imperial College, London, mop up prions, the rogue proteins that destroy the brains of people with vCJD, cows with BSE and sheep with scrapie. Hawke injected mice with prion-laden brain material from sheep that had died of scrapie. Mice injected with the antibodies up to a month later were still free of the disease after 500 days, while untreated mice all died of scrapie within 200 days. What鈥檚 more, Hawke found no trace of prions in the brains of the treated mice, suggesting they had all been mopped up.
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But mice already stricken with scrapie were not saved by the antibodies, Hawke found, suggesting that the treatment would be useless for people after symptoms appear. Writing in Nature (vol 422, p 80), the team speculates that the antibodies are too big to enter the brain and so can鈥檛 neutralise prions already there.
Just how many people might need treatment remains uncertain. The UK CJD Surveillance Unit in Edinburgh has just published figures showing that the number of cases of vCJD is falling. And a team at Imperial College has slashed its worst-case estimate of deaths in Britain from vCJD from 50,000 to 7000.
But the head of the Edinburgh unit, James Ironside, warns that all victims so far share a particular gene combination. A second wave of vCJD could still strike people with other gene combinations. 鈥淚t would be premature to say the problem is over,鈥� he says.