Alzheimer’s can be transmitted by contagion, but the risk is extraordinarily low and does not affect the people who care for the patients, according to research that has identified the first five cases of contagion of the disease described in the world.
The five affected people were infected by receiving growth hormone extracted from the brains of human corpses, a practice that has been abandoned, conclude the authors of the research, which is presented today in Nature Medicine. The brains of the cadavers contained a form of the beta-amyloid protein characteristic of Alzheimer’s, so those affected were inoculated with this abnormal protein along with growth hormone.
All of them received the treatment in childhood. Decades later, when they were between 38 and 55 years old, the protein had formed clumps in their brains and they developed Alzheimer’s.
“We are in no way saying that you can get Alzheimer’s disease. It is not transmitted by living with someone with Alzheimer’s or caring for someone with Alzheimer’s. It is only for people who have been accidentally inoculated in very unusual circumstances,” John Collinge, a neuroscientist at University College London and director of the research, declared in a teleconference press conference on Thursday.
The discovery that Alzheimer’s can be transmitted through medical treatment “raises the need to review measures to prevent accidental infections,” the researchers conclude in Nature Medicine. Although there is no longer a risk associated with growth hormone, because it was stopped being extracted from the brains of cadavers around 1985 and since then a synthetic version of the hormone has been used, it is important to “ensure the effective decontamination of surgical instruments.”
The five cases described correspond to patients from the United Kingdom. But researchers consider it likely that cases have occurred in other countries, where growth hormone extracted from corpses was also used. Even so, “they are very exceptional cases, it will be a small number of patients,” declared Collinge, who is a specialist in diseases caused by prions such as Creutzfeldt-Jakob.
In previous research, Collinge discovered that some people who had died from Creutzfeldt-Jakob after receiving growth hormone contaminated with prions also had plaques of beta-amyloid protein in the brain. However, those affected died before developing Alzheimer’s symptoms.
Collinge later found the beta-amyloid protein in growth hormone samples from cadavers. They were old samples that had never been used. She inoculated it into laboratory mice and the animals developed symptoms of Alzheimer’s, according to what she published in Nature in 2018.
The new research identifies for the first time cases of Alzheimer’s resulting from accidental inoculation of beta-amyloid protein.
The youth of those affected indicates that these are not cases of sporadic Alzheimer’s, which affects elderly people. A genetic study has ruled out cases of hereditary Alzheimer’s, which affects younger people. Therefore, the researchers conclude, beta-amyloid protein inoculation emerges as the only plausible explanation for the disease.
“This has important implications for the understanding and treatment of Alzheimer’s disease in the future,” Collinge stated. The discovery indicates that Alzheimer’s can be transmitted in a similar way to diseases caused by prions.
In both Alzheimer’s and Creutzfeldt-Jakob, accumulations of defective proteins form in the brain. In Creutzfeldt-Jakob, whose incubation period can be several decades, the initial defective protein acts as a seed that corrupts other proteins. In Alzheimer’s, where decades can also pass between the onset of neurodegeneration and the appearance of symptoms, the abnormal form of the beta-amyloid protein appears to act in the same way.
Furthermore, with the new data, the origin of both diseases follows the same pattern, with a majority of sporadic cases that manifest at advanced ages, a minority of hereditary cases that affect younger people and a very small number of accidental infections in medical environments.
“The Alzheimer’s field is not quite ready to consider it a prion disease,” Collinge stated at the press conference. “For now we refer to these things [the forms of beta-amyloid protein that transmit the disease] as seeds,” and not as prions.
