Tabloid headlines today are screaming "Alzheimer's Bombshell" and, apparently, thousands of health patients are questioning forthcoming surgery for fear they will "catch" Alzheimer's disease from surgical instruments. All because of this, in my opinion, badly-handled release of a very limited piece of scientific work which, and I quote from Ian Sample's piece in the Guardian, "found that a small number of people who died from Creutzfeldt-Jakob disease (CJD) after being treated with growth hormone taken from cadavers, developed brain changes seen in Alzheimer’s disease.
Doctors examined the brains of eight CJD patients who had received pituitary growth hormone, given predominantly to children with stunted growth until it was stopped in 1985. Six of the brains had an unusual build-up of protein called amyloid beta, which has long been linked to Alzheimer’s disease. The patients were aged 36 to 51 years old, but none carried gene variants that bring about the early onset of dementia.
John Collinge, director of the Medical Research Council Prion Unit at University College London, said the findings suggest that the hormone might have spread tiny pieces, or “seeds”, of amyloid beta, alongside the abnormal proteins, or prions, that gave people CJD."
If you read a little further into this Guardian piece you find that, although there was evidence for amyloid build-up in the deceased brains, none of them had died with any symptoms of Alzheimer's disease. The theory that they had, nevertheless, become "infected" with amyloid comes from the fact that none of the deceased CJD victims had any of the pre-disposing gene variants for Alzheimer's disease that cause early build-up of amyloid in brains. Hence the suggestion that the amyloid was "iatrogenically" introduced in infected batches of pituitary growth hormone.
Two prominent British researchers into Alzheimer's disease and prion disease, John Hardy and John Collinge, are quoted. "Speaking to the journal, John Hardy, a leading Alzheimer’s researcher at UCL, said: “This is the first evidence of real-world transmission of amyloid pathology. It is potentially concerning.” While Collinge said: "his team now suspected people could acquire amyloid beta “seeds” in three different ways: from a spontaneous, unlucky biological event, from a faulty gene or through a medical accident. He said there was no evidence that Alzheimer’s could be transmitted through blood transfusions, but added: “I think it’s not unreasonable to have a look. My concerns would be more to see if there is a risk of seeding from metal surfaces. I think that is something we ought to prioritise.”"
The problem with all this is the very precarious nature of the so-called amyloid theory in Alzheimer's disease research. Despite beta amyloid being heavily implicated as the causative agent in Alzheimer's, ever since the days of the eponymous researcher over a hundred years ago, no treatment of Alzheimer's that relies on preventing the enzymes in the chain to beta amyloid from working, or enhancing the clearance of beta amyloid from the brain, have worked. And it is well known that thousands of people have died with pin-sharp cognition, in old age, yet have been found, on autopsy, to have profound amounts of amyloid in their brains. It may very well be that amyloid is part of the "rubble" left in brains following the disease process, rather than the causative agent. Neither is there any clear collateral evidence that amyloid adhering to surgical instruments during brain operations can survive hospital sterilisation procedures.
It is a classic mis-handled and totally inappropriate scare story and, for their part in promulgating it, John Collinge and John Hardy should probably have their heads banged together.