>>11566709>>11566709>That's you posting nonsense in the same thread in order to discredit me.These are old posts you retard.
so you are now saying you have posted about copper enough to have people faking information.
Which means you are copperfag
It's nice that you deleted a post about amyloid.
You said amyloid is a normal protein, and that it can't be the cause.
Prion protein is a normal protein that can take on a conformational change to cause disease
When we talked on the discord (i know youre lying about it now) I showed you a paper that highlighted amyloid and swelling in neurons following head injury:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5837414/I also told you, there are copy number mutations that lead to triplication of APP, and that this mutation is linked to early onset familial alzheimers. I told you there are 5 other familial mutations leading to early onset alzheimers.
Both traumatic head injury and genetics are risk factors for early onset alzheimers, which isnt accounted for by a copper hypothesis.
If you have triplication, or more, of APP, which does not need copper, you get early onset alzheimers
Unless you want to suggest some retarded idea that people with triple APP just so happen to have more severe copper deficiencies, and the people they live with who don't have the mutation just so happen to not get alzheimers early just also happen to have copper deficiencies?
How about alzheimer mouse models where you give them mutant human genes or non-alzheimer genes? They have controlled diets, and would have the same copper levels, yet only mutant human genes cause alzheimer-symptoms in mice
What about taking human stem cells, turning them into neurons, and exposing some to amyloid beta? is it just chance that amyloid beta exposed cells die and non-exposed cells dont? When these cells are grown on identical medium, how can copper be the excuse?
How about studies where they break down amyloid plaques and the cell loss stops?
