[A] new paper appeared in Nature that seemed to take the evidence for the transmissibility of Alzheimer’s peptides from “circumstantial” to “experimentally produced”. It is fascinating, if unsettling, news, that further blurs the line between amyloid and prions.
Human prion diseases are rare. Prions usually form spontaneously or are inherited via faulty genes, but sometimes find their way into humans through consumption of contaminated brain or spinal cord tissue.
…[S]cientists 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
The researchers discovered the brains of seven of the eight contained, in addition to prions, peptide aggregates called Amyloid beta (Aβ for short).
The eight victims had all still been young enough that their brains would not be expected to show any signs of Alzheimer’s or cerebral amyloid angiopathy unless they had genetic risk factors. Understandably, given the implications, the scientists who studied their brains were concerned.
Read full, original post: The Case for Transmissible Alzheimer’s Grows