Should you be concerned about "catching" Alzheimer's?
In a new study published this week in the journal Nature, scientists said they have found evidence that the abnormal brain proteins associated with Alzheimer's disease could have been passed through specific medical procedures that took place decades ago. This introduces the concept, they say, that in certain circumstances, the disease may have the potential to be transmitted between people.
The findings have prompted shock headlines raising fears that Alzheimer's disease is now something that can be "caught."
But lead study author John Collinge, a professor of neurology at University College London, emphasized that there is no need for the public to be alarmed. "In no way is this suggesting that Alzheimer's disease is a contagious disease," he told reporters. "You can't catch Alzheimer's disease by living with someone with Alzheimer's disease or by taking care of someone with Alzheimer's disease."
What the study did show was that "seeds" of amyloid-beta, one of the abnormal proteins in the brain associated with Alzheimer's, may have been transmitted to a number of people through a form of human growth hormone that doctors stopped using 30 years ago.
The growth hormone, extracted from the pituitary glands of human cadavers, was injected into thousands of people of short stature between 1958 and 1985. Then studies showed that some of these samples contained prions -- proteins that can fold in multiple, structurally distinct ways that can replicate by inducing other proteins -- that caused some patients to develop Creutzfeldt-Jacob disease (CJD), an extremely rare and fatal brain disorder. Once these reports came to light, doctors stopped using the treatment.
For the current study, Collinge and his team looked at the autopsies of eight people who died of CJD, and found that in addition to the prions, six of them harbored deposits of amyloid-beta associated with Alzheimer's in their brains. It was widespread in four.
This struck the researchers as very unusual, as the patients were relatively young at the time they died -- aged 36 to 51 -- and further tests showed that none were genetically predisposed to early-onset Alzheimer's.
The researchers also said they ruled out other theories, including the possibility that having CJD would make the patients more likely to develop the amyloid-beta pathology or that the prions triggered it.
They concluded that a plausible explanation was that the amyloid seeds had been transmitted along with the CJD prions during the human growth hormone procedures.
While animal studies support this theory, Collinge noted that the current study was observational and does not prove that the procedure did in fact cause the amyloid pathology in humans. And since the patients died of CJD, it is unknown whether they would go on to develop full-blown Alzheimer's disease.
While there is no evidence that any medical procedure used today, including blood transfusions and routine surgeries, can transfer these seeds from one person to another, scientists say research should begin looking into these possibilities.
"There is no need for alarm. I don't think anyone should delay or reconsider having surgery on the basis of this data," Collinge said. "We've got no evidence at all that this is a risk to humans. But I think it would be prudent to do more research in this area going forward."
An estimated 30,000 people worldwide received human-derived growth hormone before it was replaced with synthetic hormones in 1985. As of 2012, scientists have identified 450 cases of CJD that were tied to human growth hormone injections and other medical procedures. Because of the long incubation period of at least 30 to 40 years, more cases are expected to develop. The National Prion Clinic in the UK provides resources on their website and a help line for people who may have been affected.
