Alzheimer’s can spread between people in rare medical accidents, research suggests
Research shows that Alzheimer’s disease can be spread from person to person through rare medical accidents, although experts emphasize that there is no evidence that the disease can be passed between people through daily activities or routine care.
Researchers say a handful of people who received human growth hormone from the pituitaries of deceased donors developed Alzheimer’s disease at a young age — likely because the hormones used were contaminated with proteins that seeded the disease in their brains.
“We are not for a moment suggesting that you can get Alzheimer’s. This is not transmissible in the sense of a viral or bacterial infection,” says Prof. John Collinge, co-author of the study and director of the MRC Prion Unit.
“It’s only when people have been accidentally vaccinated, essentially, with human tissue or extracts of human tissue containing these seeds, which is fortunately a very rare and unusual circumstance.”
The team says the new work adds weight to the idea that Alzheimer’s disease shares similarities with prion diseases, including in the mechanism by which the proteins involved spread through the brain.
Prion diseases, including Creutzfeldt-Jakob disease (CJD), kuru and BSE, are caused by infectious, misfolding proteins that propagate in the brain. These diseases usually occur spontaneously, but in rarer cases they can be the result of a genetic mutation or transmitted through infected brain or nerve tissue.
Writing in the journal Nature Medicine, Collinge and colleagues report how between 1959 and 1985, at least 1,848 patients in Britain received human growth hormone extracted from the pituitary glands of cadavers.
However, the practice was banned in 1985 after it was found that some patients subsequently died of CJD as a result of hormone samples contaminated with CJD-causing proteins.
Of the 80 such cases in Britain, some were also found to have a protein called amyloid beta in their brains when they died – a hallmark of Alzheimer’s disease. While it was unclear whether they would have developed symptoms of Alzheimer’s disease, other research showed that amyloid beta was present in some of the hormone batches, and that these caused an Alzheimer’s-like disease when given to mice.
Researchers reported findings from all eight people referred to the National Prion Clinic between 2017 and 2022.
They all received human growth hormone from cadavers but did not have CJD. Five had symptoms of dementia that met clinical criteria for Alzheimer’s disease, with onset as early as age 38. Three of these patients had brain scans consistent with the diagnosis, while two had biomarkers that met criteria for Alzheimer’s disease.
Of the other three patients, one had mild cognitive impairment, one had self-reported cognitive problems and one had no such symptoms, with the former showing postmortem results consistent with Alzheimer’s disease and the latter meeting biomarker criteria for the disease.
Five patients had DNA data, but only one showed a genetic risk factor for late-onset Alzheimer’s disease, and none had genetic variants known to cause early-onset Alzheimer’s disease.
The researchers add that the patients showed a number of symptoms that differed from those typical of Alzheimer’s disease, which either arises spontaneously or is linked to a genetic risk. They state that this could either be due to their disease having different origins or arising from different “strains” of the disease. amyloid beta.
The results, they say, provide evidence that Alzheimer’s disease can develop as a result of treatment with the contaminated pituitary hormone.
Although the cases involved repeated exposure to contaminated human growth hormone over a period of years, Collinge and colleagues say the findings increase the importance of measures such as ensuring effective decontamination of surgical instruments.
However, Andrew Doig, professor of biochemistry at the University of Manchester, said experts were already very cautious about transferring brain tissue between people.
Doig also cautioned that the study included only eight patients, some of whom had no genetic data, while there was no direct evidence yet of different strains of amyloid beta.
“Although the new type of Alzheimer’s reported here is of great scientific interest because it reveals a new way of spreading the disease, there is no reason to fear it since the way the disease was caused more than 40 years ago was discontinued. Doig said. “The transmission of diseases from human brain to brain in this way should never happen again.”