Louis Pasteur and Robert Koch first got to grips with assorted bacteria in the 19th century.
Later, the general rule in biology was that all pathogens contain genetic material.

THE DOGMA

until 1982

The prion theory of the American biochemist Stanley Prusiner played havoc with this dogma. In a sole-authored study in Science, he claimed that the sheep disease scrapie was triggered by altered proteins that were incorrectly folded. But proteins don’t contain any genetic material. Prusiner maintained that prions are also the pathogens that cause other unexplained diseases such as BSE.

THE HERETIC

9 April 1982

Whoever upends a dogma can expect to meet with resistance. That was also the case with Prusiner. His prion theory found adherents, but many scientists continued to believe that there is no such thing as a pathogen lacking genetic material. The problem was that Prusiner couldn’t prove that the diseased proteins can infect other proteins. One of his critics was Heino Diringer, a virologist at the Robert Koch Institute. He believed that the pathogens of BSE and Co. were in fact tiny viruses that worked very slowly.

THE WAR OF OPINION

1982-1997

French researchers published a study in ‘Science’ contradicting Prusiner’s prion theory. They infected mice with brain matter from BSE-infected cows. The mice became sick, but the incorrectly folded protein was not found in all of them. The prion only emerged when they infected healthy mice with brain cells from sick mice. They concluded that prions might play a role in infection, but are not decisive.

THE COUNTER-ARGUMENT

17 January 1997

Prusiner was awarded the Nobel Prize in Medicine for his prion theory. This surprised many people. The German medical journal Deutsches Ärzteblatt even wrote that a “daring idea is ennobled”. But the Nobel Committee “believes” Prusiner, claimed a report in the magazine ‘Spiegel’.

CANONISATION

6 October 1997

Despite the Nobel Prize, many researchers continued to doubt the prion theory. The problem always remained the same: Up to now, no one could prove that prions infect healthy proteins with their incorrectly folded form. What’s more, there is an extremely high number of different prion forms in the range of degenerative brain diseases. This was understood to be a sign that the true pathogen must be something else.

LONG-STANDING DOUBT

1997-2010

In Science, a group of researchers published the results of an experiment in which they completely isolated the sick prions, and infected wild mice with pure prions. They found the incorrectly folded prions in the diseased brains. The infectiousness of prions was now regarded as having been proven, because all of Koch’s postulates had been fulfilled: The pathogen can be cultivated outside the organism, and it alone triggers the disease.

THE PROOF

26 February 2010

The prion theory is also relevant to research into Alzheimer’s. This disease of the elderly is becoming more and more widespread, and is characterised by two incorrectly folded proteins, beta-amyloid and tau. These two suspects are believed to trigger the disease by working in tandem. Prusiner is at the forefront of the research. But after several therapeutic failures, there is considerable doubt as to whether the incorrectly folded proteins are really responsible for the disease.

HOPE AND DISAPPOINTMENT

The present

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Feature: Belief in science