The prion dilemma confounding science educators

In this paper, the issue of the prion hypothesis, a simmering controversy within the scientific community, is addressed. We inquire into the appropriateness of the use of certain augmentations and rhetoric approaches used during scientific debates, as well as the aptness of unequivocal statements in textbooks that indicate “abnormal prions” as a primary cause of Transmissible Spongiform Encephalopathies.

Creative Commons Attribution Licence permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
The author(s) declared that no grants were involved in supporting this work.

Grant information:
No competing interests were disclosed.

Correspondence
According to some in the field, one should refrain from discussions concerning controversial issues in science if one is not actively conducting experimental research 1 . We must dissent, most particularly when the prions controversy is under consideration. One does not have to conduct scientific experiments to recognize not only the flaws of the prion protein (PrP) hypothesis 2 , but the inappropriate vocabulary used during discussions of the issue. As science educators, we are still confounded when trying to present the cause of Transmissible Spongiform Encephalopathy (TSE) to our students.
To start with, for the past twenty years, the majority of biology text books unequivocally identified PrP Sc as the causative agent of TSE, and some texts even refer to the "prion hypothesis" as the "prion theory", please see Table 1. Yet, when introducing the scientific method in high schools and college classes, we establish that in order for a hypothesis to become a scientific theory, it has to be supported many times over through experimentation 3 providing a substantial and conclusive body of evidence 4 . Upon reviewing experimental work on PrP, one notes that initial studies are rarely, if ever, repeated by other scientists. Instead, they move on without giving reconsideration to the assumption upon which they base their work 5 .
When describing the scientific method, it is important that we emphasize the difference between faith and fact. Nevertheless, during discussions of the PrP hypothesis in meetings, conferences and private discussions of scientists, "I think" is too often replaced by "I believe". Perhaps, this inclination began when the Karolinka neurologist Lars Edison told The Times newspaper, upon the announcement of the Prusiner's Noble Prize: "There are still people who don't believe that a protein can cause these diseases, but we believe it" 6 . There should be no place in science for such a subjective declaration. Even recent publications emphasize that the scientific community has been split into PrP "believers" and "nonbelievers". Laura Manuelidis, one of the main scientists who rejects the PrP hypothesis, has been portrayed as a "prion heretic" 7 . Upon entering the combination of "prions" and "belief" in a Google search, we generated an astonishing 918,000 hits. Another recent tendency in modern science is marginalizing scientists as the "minority" versus the "majority", as is seen in the PrP controversy 7 , a partition more suitable for political rather than scientific discussions. the emerged discussion and conceptualization of the paper and all approved the final version of the manuscript.

Competing interests
No competing interests were disclosed.

Grant information
The author(s) declared that no grants were involved in supporting this work.
In covering the PrP hypothesis in classrooms, are we also to employ a vocabulary in which the scientific community is divided into "believers" and "nonbelievers" or "majority" and "minority" as if we were referring to a religious conviction or a political debate rather than a scientific dilemma?
Author contributions 09 September 2013 Referee Report: I agree with the authors on how important open discussion is in science. However, the prion hypothesis has been well and openly discussed for many years. Due to the hypothesis, many achievements have been obtained. Abnormal prion proteins resulting from prion protein gene mutations clearly cause genetic prion diseases.

I have read this submission. I believe that I have an appropriate level of expertise to confirm that it is of an acceptable scientific standard.
No competing interests were disclosed. The scientific community has been split in the past into those who believed the prion hypothesis and those who did not. During the 1980s and part of the 1990s, most work on the prion hypothesis was from group, and those who questioned the prion hypothesis were doing so largely by finding Stanley Prusiner's potential errors in the work of one laboratory. However, now we have hundreds of papers on mammalian PrP, including, most importantly, the demonstration that transmissible disease can be caused by a pure recombinant prion protein ( ), that are not from Prusiner and whose results are Wang , (2010) et al consistent with the prion hypothesis. In addition, work by many groups on yeast prions demonstrated the validity of the generalized prion hypothesis (inheritance mediated by conformational changes in proteins) in a more experimentally tractable system in which controls that were not possible for mammalian PrP could easily be done. So, at this point, I see no problems with the statements made in the textbooks that are listed in the Table. The prion hypothesis is as well-established, at least for mammalian PrP, as the chemiosmotic (Mitchell) hypothesis for ATP synthesis by mitochondria, which was controversial at the time it was proposed in the early 60s, but which is now the only mechanism described in textbooks. It is no longer necessary to even mention the alternative ideas from the 60s, such as chemical coupling.