Alzheimer’s disease could be transmitted during surgery and blood transfusions

“The findings from today’s study must be considered by all relevant organisations to ensure current guidance is as robust as it needs to be”. The actual reporting of the study was generally accurate and contained useful words of reassurance from independent experts.

What kind of research was this?

The observations are from a small number of deceased patients who had a treatment that hasn’t been used for years.

The aim is to advance our understanding of prion disease in the brain.

Scientists have recently discovered that there is a similarity in the process of protein misfolding between the aforementioned rare diseases and neuro-degenerative disorders like Lou Gehrig’s disease, Parkinson’s and Alzheimer’s.

What did the research involve?

He added: “Injections of growth hormone taken from human brains were stopped in the 1980s”. And, since the incubation time can be more than 40 years, individuals will not know for a very long time that their body has been contaminated. None had genetic mutations leaving them at risk for early-onset Alzheimer’s.

Unexpectedly, half of the sufferers had massive quantities of amyloid protein – this forming sticky tissues developing between brain cells that block them from interacting with each other correctly in Alzheimer sufferers. This was “substantial” in four patients. Once these misfolded prion proteins appear, they aggregate to form clumps that lead to neuronal loss and the other brain damage seen in CJD. Amyloid deposits in brain arteries can cause bleeding, strokes and dementia. None had been diagnosed with Alzheimer’s either. You can’t catch it from a patient with a disease. It is unheard of for people in this age group to have such proteins.

How did the researchers interpret the results?

The findings could suggest that the seeds of amyloid beta were spread to the patients along with the abnormal proteins that gave them CJD.

The researchers’ hypothesis is that a protein in the growth hormones, produced by the pituitary gland at the base of the brain, is to blame, and that it can be transferred from one person to another.

Worryingly the proteins which cause dementia are a type called prions which can stick to metal surfaces, such as surgical instruments, and are resistant to conventional sterilization. No other forms of prion disease were associated with beta amyloid deposits in the same way among young patients, according to the study. But it doesn’t answer those questions.

Scientists and researchers were quick to point out that the new findings are extremely preliminary, and that one can not “get” Alzheimer’s simply by being around someone who has it. All six patients died of CJD so it wasn’t possible to say whether they would have gone on to develop Alzheimer’s if they hadn’t succumbed to the prion disease.

It’s known, for example, that taking brain tissue from a mouse with Alzheimer’s disease and injecting it into healthy mice will cause the latter to develop the neurodegenerative disease.

Beta amyloid protein has likely been transmitted on rare instances to people who received human growth hormone extract made from cadavers, a study finds. But that study only looked at death certificates, not autopsy results.

Currently, low concentrations of beta amyloid seeds can’t be detected in the blood or other fluids, which is another avenue to research, Collinge said.

The paper urges further research into possible risks for “accidental” medical transmission. “There is evidence from animal studies that it is not implausible”. They include Creutzfeldt-Jakob in people, the very similar mad cow disease in cattle, and scrapie in sheep and goats, Walker says.