Call for papers: Prusiner, prions and mad cow disease
In 1982, neurologist and biochemist Stan Prusiner proposed
the prion hypothesis to explain the mechanism of infection
involved in a rare category of neurodegenerative diseases,
the transmissible spongiform encephalopathies (TSEs). The
prion hypothesis holds that the infectious agent of TSEs is
not a virus but a protein. This proposition was clearly
unorthodox and the question of whether it was breaking with
Crick’s central dogma of molecular biology was raised. The
prion hypothesis remains controversial, yet, in 1997
Prusiner was awarded the Nobel prize for Physiology or
Medicine. There is no doubt that Prusiner's research has
completely transformed the TSE field and has far-reaching
implications for biology in general. For instance, it has
recently been claimed that prions convey hereditary
information.
The dramatic changes that took place in TSE research in the
15-year gap between Prusiner's formulation of the prion
hypothesis and its full recognition are intertwinned with
equally dramatic political developments. In 1986, bovine
spongiform encephalopathy (mad cow disease) was first
diagnosed by UK scientists. In 1996, the British government
announced that the disease had transmitted to humans. This
public health crisis has now reached international
proportions. Rarely has the connection between science and
politics been so topical.
Call for papers:
We are seeking essays for an anthology examining Stan
Prusiner and the prion controversy and/or the mad cow
disease crisis. For this interdisciplinary book,
historical, rhetorical, philosophical, sociological,
linguistic, cultural, political, and anthropological
contributions are welcome. Contact Dr Eve Seguin, Dept of
History, Aberdeen University, <[log in to unmask]>
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