1982, Stanley Prusser discovered that a very simple prion protein (PrP)
seemed to be responsible for diseases such as those mentioned above.
He recognized that there were two stable forms of PrP, one composed of
alpha helices (a, above) found in nerve cells and another having beta helices
(b, above) found only in diseased mammals. He suspected that the
mutated PrP could overwhelm healthy PrP, leading to cell death and the
development of large vacuoles in brain tissue as found in spongiform encephalopathy.