Evidence is building that brain-damaging sticky proteins – central to Alzheimer’s disease and other neurodegenerative conditions – are transmissible between people under certain conditions, possibly during surgical procedures.
Such events would be rare, even freakish, and the researchers have cautioned that their findings do not suggest that Alzheimer’s and other diseases are contagious, per se.
However, they have concluded that it’s possible that the transferring of these proteins between people could cause the development of brain disease later in life. The damage may take decades to emerge.
Risk probably small
“The risk may turn out to be minor, but it needs to be investigated urgently,” lead researcher Professor John Collinge told the journal Nature, where the research was published on December 13. Professor Collinge is professor of neurology and head of the Department of Neurodegenerative Disease at the UCL Institute of Neurology, in London.
His findings follow a complex set of events that began decades ago when thousands of British children were treated with pituitary-derived human growth hormone – taken from dead donors – to treat various causes of short stature.
In 2015, Professor Collinge and colleagues examined the brains of eight of those patients, all of whom had died young – from 30s to early 50s – from Creutzfeldt-Jakob disease (CJD).
The conclusion was that CJD had been present in the growth hormone and infected the children. (The New Daily has more news to report in coming days about CJD being transmissible.)
To the researcher’s surprise, six of the dead patients had substantial amounts of amyloid-beta (Aβ), the so-called sticky plaques that build up in the brains of Alzheimer’s patients and is believed to contribute to dementia symptoms.
Seeds of trouble
Four of them were found to have suffered from cerebral amyloid angiopathy (CAA), a disease caused by the build-up of amyloid beta in blood vessels in the brain – and which can cause bleeding.
“The Aβ deposition in the grey matter was typical of that seen in Alzheimer’s disease and Aβ in the blood vessel walls was characteristic of cerebral amyloid angiopathy,” Professor Collinge and his team reported
The amyloid-beta deposits were not found in the same places where the Creutzfeldt-Jakob prions were deposited.
Professor Collinge – in what has been described as a “provocative” paper – concluded that in rare circumstances, Alzheimer’s disease might be transmissible.
“In addition to sporadic Alzheimer’s disease and inherited or familial Alzheimer’s disease, there could also be acquired forms of Alzheimer’s disease,” he wrote.
The idea was that “proteopathic seeds” of Alzheimer’s could be transmitted in the same way as the prions associated with CJD and other prion diseases.
This week, Professor Collinge and his team published a new paper in Nature that supports the earlier findings.
The researchers tracked down vials of the human growth hormone that were used in the medical treatments (discontinued in 1985).
Mice developed brain plaque in experiments
They found the some of the samples did in fact have significant levels of amyloid beta proteins (implicated in both CAA and Alzheimer’s) and tau proteins (implicated in Alzheimer’s disease). A diagnosis of Alzheimer’s disease requires detection of both aberrant proteins, amyloid beta and tau.
The researchers then succeeded in using these old samples of growth hormone to seed amyloid pathology – the build up of brain plaque – in mice.
“We have now provided experimental evidence to support our hypothesis that amyloid beta pathology can be transmitted to people from contaminated materials,” Professor Collinge said in a prepared statement.
“We cannot yet confirm whether medical or surgical procedures have ever caused Alzheimer’s disease itself in people, or how common it might be to acquire amyloid pathology in this way.”
He said that it will be important to review risks of transmission of amyloid pathology by other medical procedures still done today, including instruments used in brain surgery, “drawing on other research and what we already know about accidental CJD transmission”.
Dr Rob Buckle, chief science officer at the Medical Research Council, which funded the study, said in a prepared statement from UCL: “This study provides new insights into the molecular mechanisms underlying the role of amyloid in Alzheimer’s disease.
“However, these experiments were in mice predisposed to develop Alzheimer’s disease pathology and there is currently no evidence that AD can be transmitted between people.”