Alzheimer’s leads to a loss of brain tissue (Image: PASIEKA/Getty)
Can Alzheimer’s disease spread between people? Possibly, through a medical procedure banned in the 1980s – but some say the evidence is too circumstantial.
John Collinge of University College London and his colleagues looked at the brains of eight people who had been injected with human growth hormone as children – a therapy that around 1800 people in the UK received between 1958 and 1985.
Advertisement
The hormone had been extracted from the pituitary glands of dead donors, but it later turned out that they had been harbouring the prion disease Creutzfeldt-Jakob Disease (CJD). The eight recipients contracted CJD, via the hormone, and later died.
Now, fresh autopsies on their brains have revealed that six also had amyloid plaques similar to those seen in Alzheimer’s – even though they had died between the ages of 36 and 51, long before the disease typically develops.
Collinge believes molecules seeding the plaques were passed to the recipients via the donated growth hormone, saying the donors must have been developing Alzheimer’s as well as CJD.
Unexpected consequence?
The researchers confirmed that none of the six recipients carried known genes for developing early Alzheimer’s, which might have explained the presence of the plaques. Nor could he find evidence of the Alzheimer’s amyloid protein in the brains of 116 additional people who died of CJD or other related diseases, but who didn’t receive contaminated growth hormone. This suggests that the appearance of amyloid plaques isn’t simply an unexpected consequence of developing CJD.
The team also found amyloid protein in the pituitary gland – where growth hormone is produced – of people who had died of Alzheimer’s. This suggests that contamination is possible if growth hormone is extracted from the gland and then injected into a healthy recipient.
The good news is that it’s unlikely the disease can spread in blood, through transfusions for example, or through some common forms of surgery.
“Our current data have no bearing on dental surgery and certainly do not argue that dentistry poses a risk of Alzheimer’s disease, ” says Collinge. “Our findings might be relevant to some other medical or surgical procedures, but evaluating what risk there might be, if any, requires much further research. “
However, some researchers doubt that the new study even demonstrates that the growth hormone injections posed an Alzheimer’s risk. All six patients died of CJD so it wasn’t possible to say whether they would have gone on to develop Alzheimer’s if they hadn’t succumbed to the prion disease. Nor did any of them have signs of tau tangles, clumps of tau proteins that collect within brain cells and which are an important hallmark of Alzheimer’s disease.
What’s more, Collinge’s team couldn’t analyse samples of the growth hormone that was actually injected into the six patients to confirm whether it contained amyloid proteins.
Sceptical of a link
Because of this, David Irwin of the University of Pennsylvania in Philadelphia – whose work suggests Alzheimer’s can’t be transmitted via human growth hormone – is sceptical of a link.
“There remains no definitive evidence that clinical manifestations of Alzheimer’s can be transmitted between humans,” he says.
Mathias Jucker of the German Center for Neurodegenerative Diseases in Tübingen, Germany, also has doubts. “We have to make sure that it was really transmission,” he says. The only proof, he says, could come from experiments in which any remaining samples of the contaminated hormone are injected into mice to see if the rodents develop Alzheimer’s plaques as well.
Collinge says these samples do indeed exist, and his team hopes to perform experiments along the lines of those suggested by Jucker soon. “But the experiments take one or two years,” he says.
“If we know it was indeed transmission, we should start looking into other medical procedures where Alzheimer’s plaque material from the brain may come into contact with other patients,” Jucker says.
Jucker has previously shown that it is possible to spread Alzheimer’s to mice by injecting human amyloid brain material into the brains of the rodents. Elsewhere this week, Jucker’s team reported that amyloid seeds can remain “dormant” in mouse brains for months – at least a quarter of their lifespan – then regain their ability to cause disease. This suggests that if amyloid did somehow make it from one person’s brain to another’s, it could potentially cause disease after very long incubation intervals.
Journal reference: Nature, DOI: 10.1038/nature15369
Topics: