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Can You Catch Alzheimer’s from Growth Hormones?

Brain damage found in autopsies of patients with Creutzfeldt-Jakob disease acquired from growth hormone injections is strikingly similar to the damage done by Alzheimer’s disease.

“This study is extraordinary as it suggests that pituitary glands of humans used to make the human growth hormone contained seeds that caused the amyloid beta pathology observed. This matters enormously as it raises the possibility that other routes of transmission, including surgical instrument use and blood transfusion, could be relevant to the transmission of Alzheimer’s disease, cerebral amyloid angiopathy and other neurodegenerative diseases. There however continues to be great controversy around the mechanisms that cause Alzheimer’s disease and so the current study will be yet another one that adds to the challenging and important ongoing debate.”

Dr Bryce Vissel is the Roth Fellow Head of Neurodegeneration Diseases Research Laboratory at the Garvan Institute of Medical Research.


“While the findings of this study might imply that Alzheimer’s disease (AD) is transmitted following treatment of prion-contaminated human growth hormone, it should be recognised that this study is a relatively small observational study and thus does not show cause and effect. These findings do not allow for a definite conclusion that there is human transmission in AD. Further work is required to determine the significance of these findings and to explore other explanations, such as whether the AD pathology is a secondary effect of prion-contaminated human growth hormone treatment (i.e. inflammation).

“This interesting study needs to be followed up to determine whether amyloid beta behaves like prions to replicate itself but, irrespective of this outcome, it should be noted that neither Creutzfeldt-Jakob disease (CJD) nor AD is contagious.”

Prof Ralph Martins is Director of the Centre of Excellence for Alzheimer’s Disease Research and Care and the Foundation Chair of Ageing and Alzheimer’s Disease at Edith Cowan University.


“The numbers of cases are small (eight), but four of these did have significant amyloid beta deposition, so it comes down to an assessment of whether this is more than would be expected in an age-matched population (ages 36–51). This age span is exactly at the transition period between normality and the earliest phases of preclinical sporadic Alzheimer’s disease.

“Most importantly, there are many recipients of pituitary products from the past (approximately 2000 people in Australia received the product and four of them developed CJD), who will be concerned now whether they have an increased risk of developing AD. Our message to these recipients is that much more work is required to settle this issue. Currently, Prof Steve Collins of the Australian National CJD Case Registry is reviewing all the files of recipients who have died over the last 30 years. This work is ongoing and we will get results in the near future.”

Prof Colin Masters is Senior Deputy Director of The Florey Institute and Laureate Professor at The University of Melbourne.


“The findings are certainly interesting and warrant further investigation. Amyloid-beta protein deposition is an unusual finding in the brains of young individuals who do not have a known genetic predisposition to the disease [Alzheimer’s]. The first question to answer is whether transmission through contaminated injections is in fact possible and can lead to full blown Alzheimer’s disease (tau, amyloid-beta deposition and cell loss).

“The incubation period was extensive and progression of the disease would certainly be expected during this time if the normal disease process was underway. The diffuse amyloid-beta deposits seen would certainly not be sufficient to cause clinical Alzheimer’s disease. Whilst further research is clearly warranted, it is premature to suggest that medical procedures involving implements that had previously been used on individuals affected with Alzheimer’s disease could cause transmission of the disease.”

Dr Claire Shepherd is a Senior Research Facility Manager at the Sydney Brain Bank and Conjoint Lecturer in Pathology, UNSW.


“Proteins are long chains of amino acids. Most proteins need to fold up into a specific shape to work, sometimes this folding goes wrong and the misfolded proteins can cause disease. Examples include the beta amyloid protein – thought to play a central role in Alzheimer’s disease – and prions.

“Prions also are able to be “infectious” in that the misfolded, toxic prion protein can induce normal prion proteins to misfold into the toxic form... It has long been suspected that the misfolded

β-amyloid found in Alzheimer’s disease also has prion-like properties. Misfolded β-amyloid can convert soluble β-amyloid into toxic aggregates in test-tube experiments, and if you inject high enough concentrations into the brains of mice. However, there was no evidence that this could occur in people.

“This new paper shows that some people who were injected with human growth hormone sources from human brains, and contaminated with the Creutzfeldt-Jakob prion, developed deposits of misfolded β-amyloid in their brains.

“It is likely that the β-amyloid deposits were developed from injected misfolded β-amyloid rather than the Creutzfeldt-Jakob prion inducing the production of misfolded β-amyloid. This suggests that once misfolded β-amyloid is produced in the process of developing Alzheimer’s disease, it can accelerate its own production.

“But Alzheimer’s is not infectious in the common sense. β-amyloid has very weak prion-like activity. You would be unlikely to develop Alzheimer’s disease even if you ate the brain of someone with Alzheimer’s.”

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.

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Compiled by the Australian Science Media Centre