https://en.wikipedia.org/wiki/Major_prion_protein
Demonstrating "some other other protein behaving like a prion" is close to nobel prize territory.
ie. some protein other than PrP gets misfolded and then acts as a template to cause more misfolding. I've read up a bit on ALS as my sister has it and while it's not fully understood the most likely cause seems misfolding of a proteins called or TDP-43 or SOD1. Eg from a paper:
>recent cultured cell line and animal model studies suggest that the misfolded forms of SOD1 and TDP-43 do self-propagate within neuronal cells and transmit to neighboring cells https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4363329/
>All known mammalian prion diseases were caused by PrP until 2015, when a prion form of alpha-synuclein was hypothesized to cause multiple system atrophy (MSA).[10]
Do people who undergo spinal, brain, retinal surgery have a higher incidence of Alzheimer when compared with the rest of the population?
Otherwise there is no point in chasing this "some other other protein behaving like a prion" avenue.
In that case scarring/inflammation might trigger the Alzheimer's though. The interesting part in this article is that the growth hormone was not injected into brain tissue I assume.