It’s becoming increasingly apparent now that in the common forms of dementia like Alzheimer’s disease, similar sorts of processes are going on in the brain as happens in CJD.
Published in The Lancet Neurology: “…the interaction between PrPC and synaptotoxic amyloid-β assemblies can be efficiently blocked by PRN100 — suggesting a possible future role for anti-PrP antibodies in treating Alzheimer’s disease, and possibly other common neurodegenerative diseases.”
That is why CJD and PRN100 research are now feeding directly into Alzheimer’s science.
These 2 research publications emphasise the wider importance of researching and understanding CJD prions to potentially cure common neurodegenerative diseases.