'You Can Catch Alzheimer's': Really?

From the WebMD Archives

Sept. 11, 2015 -- People in the United Kingdom and around the world woke up to some brain-shrinking headlines Thursday morning.

“You Can Catch Alzheimer’s,” said the front page of London’s Daily Mirror

“Alzheimer’s Disease May Be Caught Through Medical Accidents,” was the headline on the Telegraph’s story.

The coverage was based on a study published in the journal Nature. The study authors suggest it might be possible -- under extraordinary circumstances -- for the same kinds of plaques seen in the brains of people with Alzheimer’s to be passed from one person to another.

We checked with the experts. Should you be worried about catching Alzheimer's disease?

“No,” says David Knopman, MD, a neurologist at the Mayo Clinic in Rochester, MN. “And then I would repeat, ‘No.’ And again, ‘No,’" he says. Knopman says he was “appalled” to see the claims made about the study.

Let’s take a look at the science.

The researchers behind the study are experts in prion diseases. Prions are responsible for a number of degenerative brain diseases, including Creutzfeldt-Jakob disease (CJD), also known as “mad cow” disease when it occurs in cows. It causes rapid memory loss, behavioral changes, a loss of vision and muscle coordination, and ultimately, death.

Prions can damage other proteins just by touching them. They can pass from one person to another through biologic products like blood and human tissue transplants. Before 1985, growth hormone injections used to treat short children were made by extracting the hormone from human tissue. In some cases, those batches of growth hormone were contaminated with prions, and some who received those injections have gone on to get the disease decades later.

The subjects in the new study were eight people between the ages of 36 and 51 who had all been treated with this contaminated growth hormone and later died from CJD.

During autopsies, doctors noticed something interesting. In addition to the tell-tale prion damage, four of the eight people also had a significant build-up of beta amyloid proteins. Sticky beta-amyloid plaques are also seen in the brains of people with Alzheimer's. Doctors use the build-up of beta amyloid along with other brain and thinking changes to help diagnose people with the disease.

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Researchers thought it was remarkable to find so much beta amyloid in people who were relatively young. They checked for genes that might explain it and failed to find any. They also wondered if the prions that caused CJD might also somehow be behind the beta amyloid build-up. They checked a group of 116 people who had died of other prion diseases, but they couldn’t find any with similar beta amyloid build-up.

That led them to conclude that the growth hormone shots must have also been contaminated with beta amyloid “seeds” that migrated to the brain and started growing and corrupting other beta amyloid proteins in the same way prions cause brain diseases.

Indeed, researchers have been demonstrating this in animals for nearly 20 years. When they take beta amyloid from the brains of people who have Alzheimer’s disease and put it into the brains of healthy mice and monkeys, they can cause sticky beta-amyloid plaques to form.

If that’s what the researchers were observing in the CJD patients, it would be the first time scientists have been able to demonstrate that beta-amyloid deposits can be passed from person to person.

But there are still some big caveats and uncertainties about what they found.

First, the patients didn’t have Alzheimer’s disease. Alzheimer’s involves the buildup of two different proteins in the brain: beta amyloid and tau. The researchers didn’t see any tau in these cases. The people also didn’t have any Alzheimer’s symptoms, though the study researchers said they might have died before they had time to develop them.

“You have to have both (beta amyloid and tau) to have Alzheimer’s disease, and they didn’t see that. None of these articles or press releases should say ‘Alzheimer’s,’” Knopman says.

Instead, what these people had was something doctors properly call beta amyloidosis. That can cause strokes and bleeding in the brain, and researchers said these patients likely would have experienced those if they had lived longer.

The distinction is critical because researchers still don’t completely understand how beta amyloid is related to Alzheimer’s. It’s not known, for instance, whether beta amyloid plaques are a cause or a consequence of the underlying disease.

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The researchers also can’t prove that the beta amyloid came from the growth hormone treatments.

Here’s what researcher John Collinge, a neurologist and head of the department of neurodegenerative disease at University College London, told reporters at a press conference Wednesday:

“This is an observational study. We’re simply describing what we see in these patients and trying to explain that,” he said. “It doesn’t prove that it was the growth hormone injections that caused their Alzheimer’s pathology.”

Collinge noted that there are still archived samples of the growth hormone in question. He’s been in discussions with Britain’s Department of Health to run tests on those samples for beta amyloid. That would go a long way toward supporting his theory.

It’s worth noting that a study by U.S. researchers published in 2013 found no evidence of an increased risk for Alzheimer’s disease in a database of more than 6,000 people known to have received the human tissue-derived growth hormone treatments.

And what about claims in the news that blood transfusions and surgical procedures might be risky, since they could, in theory, pass beta-amyloid plaques from one patient to another?

There’s no evidence of that, says Lary Walker, PhD, a neurologist at Emory University in Atlanta who wrote an editorial on the study.

“There have been a few studies that have looked at blood transfusions, and in people with a history of blood transfusions is there a higher risk for Alzheimer’s disease, and the answer is no,” Walker says.

There’s no evidence that dental procedures raise the risk, either.

“I think there’s no reason the average person should be concerned about this,” he says.

Instead, he says the study raises an interesting question that deserves more exploration.

The study authors agree.

“I think it does call for further research to be done,” Collinge says.

WebMD Health News Reviewed by Michael W. Smith, MD on September 11, 2015

Sources

SOURCES:

David Knopman, MD, neurologist, Mayo Clinic, Rochester, Minn.; vice-chair, medical and scientific advisory council, Alzheimer’s Association.

John Collinge, neurologist and head of the department of neurodegenerative disease, at University College London, London.

Lary Walker, PhD, a neurologist, Emory University, Yerkes Research Center, Atlanta.

Press conference, Nature.

Nicoll, A. Nature, Sept. 10, 2015.

Jama Neurology, April 2013.

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