Stay up to date with notifications from The Independent

Notifications can be managed in browser preferences.

Nobel prize for BSE theory scientist

Charles Arthur
Monday 06 October 1997 23:02 BST
Comments

Your support helps us to tell the story

From reproductive rights to climate change to Big Tech, The Independent is on the ground when the story is developing. Whether it's investigating the financials of Elon Musk's pro-Trump PAC or producing our latest documentary, 'The A Word', which shines a light on the American women fighting for reproductive rights, we know how important it is to parse out the facts from the messaging.

At such a critical moment in US history, we need reporters on the ground. Your donation allows us to keep sending journalists to speak to both sides of the story.

The Independent is trusted by Americans across the entire political spectrum. And unlike many other quality news outlets, we choose not to lock Americans out of our reporting and analysis with paywalls. We believe quality journalism should be available to everyone, paid for by those who can afford it.

Your support makes all the difference.

The theory that explains BSE and CJD, and maybe Alzheimer's and Parkinson's disease, has won its progenitor the Nobel Prize for Medicine. So are scientists delighted that "prion theory" is now part of the establishment? No - even its backers are surprised. Charles Arthur, Science Editor, explains why.

The Nobel Prize committee surprised scientists yesterday by awarding its Medicine prize to Stanley Prusiner, the American whose controversial "prion" theory explains a wide class of brain disorders including Creutzfeldt- Jakob Disease (CJD) and BSE, or "mad cow disease". The awards committee of the Karolinska Committee said the 7.5 million kroner prize (pounds 600,000 ) was made for discoveries that could lead to new treatments of dementia- related diseases, including Alzheimer's and Parkinson's disease.

Although prion theory is increasingly being extended to other diseases, yesterday's announcement caught even backers of Dr Prusiner off-guard. John Collinge of St Mary's Medical School, one of the main British proponents of prion theory, said: "I was expecting it [to be awarded to Prusiner] later."

The reason is that important parts of the theory remain unresolved, such as the exact processes by which illnesses like BSE and CJD spread, and what characteristics determine infectiousness. Nor has anyone ever isolated a "prion" or shown it in action.

Normally, Nobel Prizes are awarded years - or even decades - after the scientific establishment accepts an idea, and its importance to current work is recognised. Francis Crick and James Watson did not receive their Nobel Prizes for Medicine until 1962, for the structure of DNA - determined in 1953.

By contrast, Prusiner's theory has many outright opponents. He broke his long- standing refusal to talk to the media yesterday, noting dissent about his theory to say that "no single prize vindicates it ... for new ideas in science it's very important that the process move slowly and progressively."

He began working on the subject 25 years ago, after one of his patients died of CJD. He now teaches biochemistry at the University of California, San Francisco.

Contrary to conventional biology, prion theory says some infectious diseases are not caused by "living" organisms such as bacteria or viruses, which have their own genetic material, but instead by inanimate proteins.

Health officials are looking for blood donated by three people now known to have CJD and attempts are being made to trace the blood from a fourth donor suspected of having v-CJD. But Sir Kenneth Calman, the Chief Medical Officer, stressed there is no scientific evidence to suggest the disorder can be transmitted via blood transfusions or products.

Join our commenting forum

Join thought-provoking conversations, follow other Independent readers and see their replies

Comments

Thank you for registering

Please refresh the page or navigate to another page on the site to be automatically logged inPlease refresh your browser to be logged in