There has been concern in the past that some of the pathological hallmarks of Alzheimer's disease may be transmissible from human to human. A new study is adding weight to that possibility, providing experimental evidence that in the past amyloid beta plaques may have been seeded in a patient's brain through contaminated samples of human growth hormone.

This incredibly specific piece of new research follows on from a 2015 study that found signs of amyloid beta plaques in patients that had died from Creutzfeldt–Jakob disease (CJD). These patients had all received doses of specific batches of cadaveric human growth hormone that were subsequently discovered to have been contaminated with amyloid beta proteins. The hypothesis was that these contaminated human growth hormone samples may have seeded plaques in the CJD patients, implying that this major pathological hallmark of Alzheimer's disease could be transmissible.

In order to experimentally validate this hypothesis, the researchers obtained several samples of the specific contaminated human growth hormone from the prior study that had been in storage since the 1980s. Amyloid beta proteins were confirmed as present in the samples.

The researchers then administered those hormone samples to mice genetically modified to develop amyloid beta plaques. Compared to a control group of mice administered a more modern, synthetic recombinant human growth hormone, the mice given the contaminated hormone developed significantly more amyloid beta plaques.

So what does all this ultimately mean? Not necessarily all that much.

The research contains a large assortment of disclaimers, and it is important to point out that it has been decades since doctors administered these kinds of hormone preparations to patients. Back in the mid-20th century, human growth hormone was collected from the pituitary glands of cadavers during autopsies. So anyone taking hormones today need not worry, we haven't done that since the 1980s.

Bryce Vissel, from Sydney's University of Technology, suggests this new study is only of interest from a very narrow scientific perspective and should not concern anyone that may be taking human growth hormones.

"It is important to note however that first, the preparation was directly injected into the brains of mice, while in humans it was given as an injection into the blood," says Vissel, underlining several reasons why the study isn't that relevant to human patients. "Second, the mice were genetically predisposed to develop angiopathy and plaques. Third, in the humans, only mild cerebral amyloid angiopathy and plaques were seen 20-30 years later, which did not meet the criteria for Alzheimer's disease."

So, all this adds up to a highly specific set of conditions that may only mildly enhance a pathological hallmark associated with Alzheimer's disease. The researchers behind the new study do stress that this work does not at all suggest Alzheimer's is contagious, or even transmissible by blood transfusion.

However, there is an implication that Alzheimer's risk may be increased through something called iatrogenictransmission, which is when an illness is transmitted through medical examinations or treatment. In this case, the hypothetical concern is surgical instruments could retain seeds of amyloid proteins that can subsequently be transferred into patients during neurosurgical procedures.

Ultimately, this new study may be academically compelling but it doesn't demonstrate Alzheimer's to be a directly transmissible disease. While it may conclude that amyloid proteins could be seeded in a human brain, it doesn't imply the condition is contagious in any way.

The new study was published in the journal Nature.

Source: Scimex