Possible Evidence That Protein Linked To Alzheimer's Is Transmissible

The build up of amyloid beta proteins plaques has been linked to the development of Alzheimer's. Juan Gaertner/Shutterstock

New research has found possible evidence that tiny fragments of a protein that has been linked to Alzheimer’s might be transmissible. Some have even gone on to suggest that this could mean that these "amyloid beta" proteins could be spread by surgery and even dentistry, but experts have been very quick to point out that no evidence for this exists.

“I don't think there needs to be any alarm that we're saying in any way that you can catch Alzheimer's disease,” says John Collinge, who coauthored the study published in Nature. “This relates to a very special situation where people have been injected with essentially extracts of human tissue.”

The potential risk for the “transmission” of Alzheimer’s was raised when the researchers from University College London were conducting post-mortems on the bodies of eight people who had died of Creutzfeldt-Jakob disease (CJD). All of them had received injections of human growth hormones during their childhood to treat dwarfism, which were harvested from the pituitary glands of thousands of cadavers.

This practice was stopped in 1985, after the realization that the procedure could spread CJD. But the scientists noticed that in seven of the eight bodies there were deposits of amyloid beta proteins in the brain, which have been linked to the development of Alzheimer’s. This caught the attention of the researchers, as such deposits are normally only seen in elderly people, whereas the bodies in question ranged from 36 to 51 years old.

“In a sense you could say that this is an obsolete experiment,” Simon Ridley, Head of Research at Alzheimer’s Research UK, told IFLScience. “Because the growth hormone which is administered nowadays is made from recombinant [DNA], it doesn’t come from cadaver tissue as it was prior to 1985.” While the experiment might be obsolete in terms of medical procedures that take place today, Ridley acknowledges that the study is important and useful in helping to broaden our understanding of how amyloid beta behaves in the brain. 

Ridley also stressed that current procedures since the CJD scare in the 1980s already minimize any potential risk of transmission. “It's a long way to go from worrying about a purified extract from brain tissue, to worrying about surgery and dentistry, which some of the media are doing, and that’s wrong.” 

As the patients unfortunately had CJD and died mid-life, it is impossible to know whether the amyloid beta proteins would have gone on to cause Alzheimer’s, which usually only manifests later in life. The fact that the scientists only found deposits of amyloid beta and not of another protein associated with Alzheimer's, tau (both amyloid beta and tau protein tangles need to be present to definitively diagnose someone with the disease), adds further questions as to whether they would have gone on to develop Alzheimer’s.  

The overwhelming message from Alzheimer’s Research UK and other experts in the field is one of reassurance. People should not cancel hospital appointments or surgery on the back of this research, it simply adds an interesting point in the study of the disease which affects an estimated 46.8 million people globally.   

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