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Five of eight British children who received human growth hormone from the pituitary glands of deceased donors went on to develop early-onset Alzheimer's disease many decades later, researchers report.
Researchers at University College London (UCL) suspect that the growth hormone received by these people in childhood may have contained amyloid-beta protein plaques, which build up in the brains of people with Alzheimer's disease over time.
Their finding suggests that -- in very rare contexts like these -- the brain-robbing disease could be transmitted person-to-person.
However, "there is no evidence that amyloid beta can be transmitted in other contexts -- for example, during activities of daily life or provision of routine care," wrote a team led by Dr. John Collinge. He's a professor of neurology and head of the department of neurodegenerative disease at the UCL Institute of Neurology.
The findings were published Jan. 29 in the journal Nature Medicine.
As explained by the researchers, between 1959 and 1985 British children with growth issues were sometimes treated with human growth hormone that was extracted from the pituitary glands of cadavers.
However, doctors worldwide put a halt to the practice when it came to light that these procedures could transmit a type of misfolded protein called a prion, which in turn could trigger a deadly degenerative brain disorder called Creutzfeldt--Jakob disease (CJD).
When seen in animals, the illness is nicknamed "mad cow disease."
Autopsies conducted by Collinge's team showed that some patients who'd died of CJD in this way also showed signs of Alzheimer's amyloid-beta buildup.
Other studies conducted by the same team showed that cadaver-sourced growth hormone stored in labs did, in fact, contain amyloid-beta. When these hormone samples were injected into mice, the rodents went on to develop a pathological buildup of amyloid-beta in their brains.
All of this spurred Collinge's team to track the brain health histories of eight Brits who had received cadaver-sourced hormone as kids, but who were spared CJD.
Five of the eight people went on to develop early-onset Alzheimer's disease, defined as onset of symptoms between the age of 38 and 55, the researchers found. These people had dementia symptoms severe enough to impair daily living, Collinge's team reported.
Of the remaining three individuals, one developed symptoms of mild cognitive impairment (often a precursor to Alzheimer's) by the age of 42, another showed non-definitive "subjective" cognitive symptoms, while the other showed no signs of cognitive impairment, the study found.
Five of the patients underwent genetic testing which ruled out the possibility that any of them had an inherited form of early-onset Alzheimer's.
All of this suggests "that Alzheimer's and some other neurological conditions [can] share similar disease processes to CJD," Collinge said in a UCL news release. "This may have important implications for understanding and treating Alzheimer's disease in the future."
The research team stressed that people should not be alarmed by their findings: Person-to-person transmission of Alzheimer's disease remains incredibly rare.
"It is important to stress that the circumstances through which we believe these individuals tragically developed Alzheimer's are highly unusual, and to reinforce that there is no risk that the disease can be spread between individuals or in routine medical care," said study co-author Jonathan Schott, a consultant neurologist at UCL Hospital. He is also chief medical officer at Alzheimer's Research UK.
"These findings do, however, provide potentially valuable insights into disease mechanisms," Collinge said. The findings "pave the way for further research which we hope will further our understanding of the causes of more typical, late onset Alzheimer's disease."
There could be one practical consequence of the new study: An increased vigilance around the use and sterilization of medical instruments.
"The recognition of transmission of amyloid-beta pathology 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," Collinge said.
Writing in a Nature Medicine News & Views commentary, Dr. Mathias Jucker, of the University of Tubingen in Germany, and Lary Walker, of Emory University in Atlanta, said the study raises interesting points.
First of all, they said, "it is imperative to stress that Alzheimer's is not a contagious disease," and almost always emerges spontaneously within individual brains.
However, they agreed with the British team that the, "report reinforces the potential of amyloid-beta seeds as targets for early prevention, and it underscores the importance of informed caution in the preparation of surgical instruments, handling of tissues and implementation of therapeutic biologics, particularly those derived from human sources."
More information
Find out more about Alzheimer's disease at the Alzheimer's Association.
SOURCE: University College London, news release, Jan. 29, 2024; Nature Medicine, Jan. 29, 2024