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Alzheimer’s passed to patients from corpses

An Alzheimer's brain (left) compared with a healthy brain
An Alzheimer's brain (left) compared with a healthy brain - PASIEKA

Alzheimer’s disease was passed to patients given hormones extracted from corpses, scientists have shown for the first time.

Five people are believed to have developed Alzheimer’s after they were treated with a human growth hormone that inadvertently contained the seeds of dementia.

The tainted hormone was given to more than 1,800 children of short stature in the UK between 1959 and 1995 before being withdrawn when it was shown to trigger Creutzfeldt-Jakob disease (CJD).

Now, scientists at University College London (UCL) have found that the same batch responsible for cases of CJD also appears to have triggered Alzheimer’s in some patients. The youngest developed dementia symptoms at just 38 years old.

Professor John Collinge, director of the UCL Institute of Prion Diseases and a consultant neurologist, lead author of the research, said: “We are not suggesting for a moment you can catch Alzheimer’s disease. You can’t catch it by being a carer or living with a husband or wife with the disease.

“The patients we have described were given a specific and long-discontinued medical treatment which involved injecting patients with material now known to have been contaminated with disease-related proteins.

“However, the recognition of transmission in these rare situations should lead us to review measures to prevent accidental transmission via other medical or surgical procedures, in order to prevent such cases occurring in future.”

Amyloid-beta proteins found in hormone

British scientists initially stumbled across the discovery while studying the brains of eight people who died of CJD after being injected with a human growth hormone.

Unexpectedly, four of the patients had huge levels of amyloid beta protein – a sticky deposit that forms among brain cells and stops them communicating with each other properly.

Although none had developed dementia, scientists say it is likely they would have, had they lived longer.

Researchers then tracked down the original growth hormone which had been stored by the Department of Health, and found it contained the misfolded amyloid-beta proteins implicated in Alzheimer’s.

When they injected the banned hormone into the brains of mice, the animals began to develop the signs of neurodegenerative disease.

Scientists discovered that five people treated with the hormone have developed the symptoms of Alzheimer’s disease despite being aged just 38 to 55. None were at genetic risk for the condition.

First author Dr Gargi Banerjee, of the UCL Institute of Prion Diseases, said: “We have found that it is possible for amyloid-beta pathology to be transmitted and contribute to the development of Alzheimer’s disease.

“This transmission occurred following treatment with a now obsolete form of growth hormone, and involved repeated treatments with contaminated material, often over several years. There is no indication that Alzheimer’s disease can be acquired from close contact, or during the provision of routine care.”

Amyloid proteins come in different strains

It is thought that the misfolded amyloid proteins clump together in “stacks” that grow over time until they get so long that they snap, creating new “seeds”.

Each seed continues to grow, until this unfettered accumulation of amyloid in the brain starts to kill brain cells.

Dr Susan Kohlhaas, executive director of research and partnerships at Alzheimer’s Research UK, said: “This study has revealed more about how amyloid fragments can spread within the brain, providing further clues on how Alzheimer’s disease progresses and potential new targets for the treatments of tomorrow.”

There have been no reported cases of Alzheimer’s acquired from any other medical or surgical procedures but the experts said it was important to review measures and possibly bring in better decontamination methods for surgical equipment.

The team also discovered that the amyloid proteins come in different strains, like viruses, and drugs which target the main strain could allow less dominant forms to develop, which are untreatable.

Co-author Professor Jonathan Schott, honorary consultant neurologist at UCL, said: “These findings provide potentially valuable insights into disease mechanisms, and pave the way for further research which we hope will further our understanding of the causes of more typical, late-onset Alzheimer’s disease.”

Commenting on the new research, Dr Richard Oakley, associate director of research and innovation at the Alzheimer’s Society, said: “It is not known how common Alzheimer’s transmission was in the 1,800 people who had this treatment and the study only looked at the records of eight people.

“Nowadays, patients receive synthetic alternatives which have been approved for safety and do not pose a risk of transmitting diseases.”

The research was published in the journal Nature Medicine.