The problem? They’re wrong.
“The headlines were a bit of a shock this morning,” said Simon Mead, a researcher at the Institute of Neurology at the University College London. His study, published in the latest volume of Nature, inspired those front-page shockers, published beside news of Queen Elizabeth becoming the longest-serving British monarch.
“The poor queen,” Mead said.
In fact, the study contradicts much of what’s in those “bombshell” headlines. In the study, the authors conclude that there is “no suggestion that Alzheimer’s disease is a contagious disease and no supportive evidence from epidemiological studies that Alzheimer’s disease is transmissible, notably by blood transfusions.” The scientists called for more research on a phenomenon they discovered among a tiny number of Creutzfeldt-Jakob disease patients who had once been treated with the same human growth hormone.
In the paper, researchers wrote that four of the eight patients autopsied showed the presence of an abnormal protein that is also found in the brains of Alzheimer’s patients. It might suggest that in this one unusual circumstance, an element of Alzheimer’s — an element, not Alzheimer’s itself — could have been transmitted from human to human. The authors conclude it needs more research.
This is a scientific paper, after all, not one that’s meant to change consumers minds about their own health care. It’s titled: “Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy.”
Here are all the very large caveats that go with this paper’s conclusion.
First, researchers caution their findings cannot be applied to the general population.
The patients that scientists studied were among 30,000 people — mostly young boys — who were treated with human growth hormone from the pituitary glands of cadavers because they were short. Doctors stopped using this treatment in 1985 after it was discovered that a disproportionately large number of these patients had Creutzfeldt-Jakob disease. CJD is a rare, degenerative brain disorder that typically impacts only one in every 1 million people per year world-wide, according to the National Institutes of Health. It was believed that the deadly CJD proteins were transferred along with the hormone.
None of the patients they studied actually had Alzheimer’s before they died.
The authors of this paper also theorize that the seeds of beta amyloid, the abnormal protein, were also transferred along with CJD protein; hence a part of the population they studied saw an abnormal buildup of a protein that is also typical in the brains of Alzheimer’s patients. It’s a phenomenon the study authors label “unquestionably concerning,” but they again caution that more research needs to be done.
Earlier research has shown that CJD and other diseases, known as prion diseases, have been known to pass onto humans through a range of surgical and medical procedures. Other studies have shown cannibals in Papua New Guinea get prion diseases after eating diseased brains. So far, only animal studies have shown that the Alzheimer’s protein can be transferred from one animal to the other.
“Previously when amyloid-beta was injected in a mouse brain, it spread,” said Dr. Rudy Tanzi, a Harvard scientist who is best known for mapping the first Alzheimer’s gene. It’s possible the process used to isolate and concentrate the human growth hormone might have spread both proteins.
“This would not mean you could spread amyloid by blood transfusions or another method of contagion.”
Tanzi, whose lab continues to try to understand how Alzheimer’s operates, is also trying to raise money to fund Alzheimer’s research. Some 5.3 million Americans now have Alzheimer’s.
“The onus is on the authors of this new study to show that the amyloid was actually transmitted via surgery,” as opposed to developing as a normal part of CJD, Tanzi said. “With only eight cases, it is very difficult to conclude the Alzheimer’s amyloid was actually transmitted by surgery. Much more work would need to be done to confirm this.”
The authors did look at 120 other prion disease cases and did not find the accumulation of the protein associated with Alzheimer’s.
A second major caveat is that a bunch of abnormal plaque in a person’s brain does not necessarily mean that person will get Alzheimer’s.
“Many people pass away with these deposits who never develop the disease,” said Keith Fargo, the director of scientific programs and outreach for the Alzheimer’s Association. Scientist don’t know if the plaques themselves cause Alzheimer’s, or if they are a by-product of the Alzheimer’s development. Alzheimer’s patients also have Tau tangles. Tangles are abnormal collections of twisted protein threads within nerve cells. The third element is the loss of connections between neurons. When the connections are lost, the neurons start to die and the brain starts to atrophy.
The authors of the new paper suggest that the patients they studied may not have lived long enough to have developed the other elements of Alzheimer’s. The patients were between the ages of 36 and 51 when they died from CJD.
“We are not saying Alzheimer’s is a prion disease, we are saying that it may share the fundamental mechanism that something goes rogue and spreads around the disease,” said Mead, one of the authors of the study published in Nature. This “gives us strong clues that one day may help us better treat these disorders.”
What has been lost in the headlines, Mead adds, is that because they were treated with that human growth hormone, “around 30,000 who got this treatment may be at risk for other problems,” such as strokes and brain bleeds. The scientist developed a FAQ page to further explain these conclusions and hopefully clear up any confusion.
“The idea that Alzheimer’s is contagious is absolute rubbish,” Mead said. “The last thing we want to do is cause panic or cause people to avoid surgery or a blood transfusion.”