Australasian Science: Australia's authority on science since 1938

More evidence that Alzheimer's-like brain damage can be 'caught'

By AusSMC

It is possible that amyloid beta pathology, a hallmark of Alzheimer's disease, can be transmitted through contaminated human growth hormone.

A study published in Nature (see the link below) found that specific batches of contaminated human growth hormone, linked to the death of several patients from Creutzfeldt-Jakob disease (CJD) were also contaminated with amyloid beta protein, a substance thought to play a role in the development of Alzheimer's disease. When the samples were injected into mice, they produced a amyloid beta pathology, providing evidence that amyloid beta pathology can be transmitted through human growth hormone. Previous research had suggested this may be possible after patients who died of CJD were also found to have brain damage similar to that found in Alzheimer's disease.


Dr Ian Musgrave is a Senior Lecturer in the Faculty of Medicine, School of Medicine Sciences, within the Discipline of Pharmacology at the University of Adelaide.
"Alzheimer’s disease is the major dementing disease in Australia and the world, taking a terrible toll on patients and their families.

One of the hallmarks of AD is the accumulation of an insoluble protein in the brain, beta amyloid. Beta amyloid is toxic to brain cells, and is thought to be important in the development of AD, yet every therapy we have thrown at AD based on removing amyloid has failed, prompting a rethink of its importance.

These new finding bring beta amyloid back into the spotlight. We have known the beta amyloid is a prion like protein for some time. Prion proteins are responsible for diseases such as Kuru, Creutzfeldt-Jackob disease and “mad cow” disease. Prion proteins are misfolded, toxic versions of normal proteins that can act as seeds causing the normal proteins to misfold into the toxic versions in a slow but lethal cascade.

While beta amyloid has prion-like properties, this was considered largely irrelevant to AD (as we don’t eat the brains of our elderly).

In this recent work researchers have isolated beta amyloid from vials of human growth hormone derived from human cadavers that were given to people who later developed an AD like disease. Injecting these beta-amyloid containing preparations into the brains of mice that have been genetically modified to express human beta amyloid caused them to develop the same AD like disease.

This suggests that beta-amyloid does play a central role in the development of AD, and we now must investigate why anti-beta amyloid therapies have failed more closely."


Professor Bryce Vissel is Roth Fellow and the Director of the Centre for Neuroscience and Regenerative Medicine at University of Technology, Sydney.
"The study suggests that amyloid beta, when present as a small contaminating substance in preparations of hormones given to children over the period 1958-1985, can seed amyloid plaques in the brain of mice. While interesting scientifically this study has no implications for children or adults taking hormone preparations today. This is because hormones are prepared today in a very different way now, compared to how hormones were prepared in 1958-1985. The hormone in those days was prepared from the brains of cadavers, so the hormone preparation was not pure as it is today where it is made by more sophisticated methods.

This study is of interest scientifically because it shows that amyloid from those very old preparations of contaminated hormone, when injected into brains of mice, can seed increased amyloid deposition in mice. Therefore the study suggests, but does not prove, that that amyloid can act as a kind of infectious agent: the amyloid in the contaminated hormone preps could possibly have been the cause of the cerebral amyloid angiopathy and plaques seen in some humans that received the contaminated hormones twenty or thirty years earlier.

More details:

Growth hormone was once prepared by extracting it from the brains of cadavers and then was given to children that needed growth hormone. The hormones prepared this way were of course not absolutely pure and some of the batches contained small amounts of amyloid. Some children receiving batches of the contaminate hormone in 1958-1985, went on to develop evidence of mild cerebral amyloid angiopathy and plaques 20-30 years later, though this did not meet the criteria for Alzheimer’s disease.

In this study, old contaminated batches of the hormone from 1958-1985 that were pulled out from the freezer, were able to seed cerebral amyloid angiopathy and plaques in mice that were genetically predisposed to get these plaques. 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. 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 this study shows that the amyloid from the contaminated hormones are able to seed plaques and provides suggestion, but does not prove, that amyloid in the contaminated hormones were the cause of the cerebral amyloid angiopathy and plaques in the humans. However given hormones are prepared very differently today, this is not relevant for anyone taking hormones today."