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Scientists have shed new light on how Alzheimer’s spreads through the brain and found the first evidence of transmission between people, via a now-banned human growth hormone.
The study, published in Nature Medicine on Monday, looked at a small group of people who were among at least 1,848 patients treated between 1959 and 1985 with a growth hormone extracted from cadavers.
The scientists found that some of the overall cohort died from the Creutzfeldt-Jakob disease (CJD) brain disorder because their hormone infusions contained proteins called prions that cause severe abnormalities in the brain.
The findings show parallels between the evolution of Alzheimer’s and CJD, potentially boosting research into diagnostics and therapies to combat all forms of dementia.
“Our findings suggest that Alzheimer’s and some other neurological conditions share similar disease processes to CJD,” said John Collinge, the research’s lead author and a professor at University College London.
“This may have important implications for understanding and treating Alzheimer’s disease in the future,” he added.
The World Health Organization estimates that dementia affects more than 55mn people worldwide.
Collinge and his colleagues examined eight people who had received the hormone as children but did not develop CJD. However the scientists found that five of these patients showed symptoms consistent with early-onset Alzheimer’s.
Biological and autopsy studies supported an Alzheimer’s diagnosis in three of the patients and were suggestive in a fourth.
The researchers stressed they did not find evidence that Alzheimer’s was transmissible in daily life or ordinary medical care.
The findings suggested the patients’ growth hormone treatment had been contaminated with proteins of a type known as amyloid-beta, the researchers said.
These proteins, which stick together and form plaques harmful to brain cells, are increasingly regarded as a leading cause of Alzheimer’s.
The research’s sample size was small but the scientists said its outline of a new mechanism for Alzheimer’s onset would inform the quest to develop diagnostics and treatments for the disease.
A study published last week said a commercially available blood test had shown high levels of accuracy in early detection of tau, another type of protein implicated in causing Alzheimer’s.
“There is evidence that amyloid-beta aggregates can travel across synapses in the brain, spreading dementia,” said Andrew Doig, professor of biochemistry at the University of Manchester, who was not involved in the Nature Medicine paper. “This work adds support to this idea.”
The researchers behind the paper said it would be important to review medical safeguards, to ensure there was no risk of accidental contamination of patients with amyloid-beta proteins through procedures previously implicated in CJD transmission.
The human growth hormone treatment was outlawed after it was linked to CJD, with synthetic substitutes now used instead.
“There is no evidence to suggest that [Alzheimer’s] can be passed through any other route, such as day-to-day activities or routine medical procedures,” said Susan Kohlhaas, executive director of research and partnerships at the Alzheimer’s Research UK charity.
“But 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,” she added.
