In the original Alzheimer’s transmissibility study, scientists examined the brains of eight patients treated with prion-contaminated human growth hormone as children who decades later died from prion disease (out of over 30,000 people so treated, more than 200 died this way).
The hormone had become contaminated with prions because it had been extracted from cadavers — one or a few of whom presumably died of prion disease — and processed in such a way that the prions remained. Of course, prions are not the only misfolded proteins that potentially lurk in the brains of cadavers.
The researchers discovered the brains of seven of the eight contained, in addition to prions, peptide aggregates called Amyloid beta (Aβ for short). Aβ is a collection of misfolded peptides whose correctly folded versions are present in the human brain and perform a variety of mid-level tasks. When the misfolded versions form, they behave like prions, catalyzing the conversion of healthy forms into diseased ones and accumulating in clumps called plaques.