The anti-malaria drug quinacrine does not appear to extend the lives of people with the human form of mad cow disease, despite encouraging results from experiments with mice, British researchers said on Tuesday.

Their study of 107 volunteers showed some people who took the drug showed some improvement but that it was not possible to tell whether this was due to the medicine, researchers said.

The patients had Creutzfeldt-Jakob disease or CJD, a fatal brain-wasting illness in a family of diseases called prion diseases.

These include mad cow disease or bovine spongiform encephalopathy, scrapie in sheep, and a new form of CJD that has infected fewer than 200 people worldwide who ate BSE-contaminated meat products.

"After adjusting for the substantial differences between patients who chose to take quinacrine or not, we did not find any evidence that oral quinacrine at a dose of 300 mg a day increased the length of survival of patients with prion disease," John Collinge of University College London and colleague wrote in the journal Lancet Neurology.

Currently there are no drugs that prevent or reverse the disease, though quinacrine has shown promise in treating prion-infected mouse cells because it can penetrate the blood-brain barrier, the researchers said.

The drug has been effective in treating these prion-infected mouse cells by blocking the conversion of normal proteins into the abnormal disease-causing form, the researchers said.

Human prion diseases can arise spontaneously, be inherited through a genetic mutation or develop through infectious transmission via contaminated meats, biological and pharmaceutical products or cannibalism.

They are passed along by misfolded infectious protein fragments called prions.

A very rare disease called variant CJD has been found in people who ate infected beef products. Fatal and incurable, it has affected fewer than 200 people so far. A genetic mutation causes CJD in one in a million people globally.

Collinge and his team offered patients a choice of quinacrine. Seventy-eight people died during the study.

Yet the study does show it is possible to conduct trials for rare, rapidly progressive and fatal diseases, Michael Geschwind of the University of California, San Francisco, wrote in a commentary.

"Future studies will need a design that provides unequivocal answers on treatment efficacy," he wrote in the Lancet Neurology.