This computer artwork shows the brain’s neural network represented by lines and flashes. A new study indicates Alzheimer’s markers in the brain may have been spread via a protein. Photo by Alfred Pasieka/Science Photo Library and Getty Images
From 1958 to 1985, 30,000 people worldwide were exposed to a contagious, highly fatal brain disorder called Creutzfeldt-Jakob disease. These infections were caused by by a malevolent protein — called a prion — that was unknowingly present in human growth hormone treatments given to these patients. (Most were children with growth defects.) Because the disease can take decades to manifest, the fallout continues, with the most recent of 229 deaths occurring just three years ago.
Today, scientists from England report another possible consequence of these tainted hormone treatments: Alzheimer’s disease. When they examined postmortem tissue from eight of these Creutzfeldt-Jakob disease patients, they found amyloid-beta plaques, one of the marquee features of Alzheimer’s disease, spread widely across some of the brain specimens.
“What we find, very much to our surprise, is that of these eight patients, four of them are really quite significant in severe deposition of Alzheimer amyloid protein in their brain, so-called beta-amyloid,” said University College London neurologist John Collinge, who led the study published today in the journal Nature. Three other patients had small to patchy amounts of amyloid-beta in their brains. Four of the patients also had a form of blood vessel damage — called cerebral amyloid angiopathy — that is seen with Alzheimer’s disease.
This study does not suggest that Alzheimer’s disease is contagious or a threat to the blood supply, but the findings do raise a longstanding question of whether amyloid-beta proteins can behave like prions. If they do, the protein could pose a contamination risk to hospitals, given Alzheimer’s patients and their biological samples are not treated with the same biohazard protocols as those with prion disease.
Prions are nuggets or aggregates of misfolded protein. Protein aggregates are normal in the brain, but prions are special because they’re sticky. Like a snowball rolling down a mountain, they can grow by having other proteins cling to them. But as they build, they destroy brain cells, ultimately carving spongelike holes into the central nervous system.
People have implicated prions in Alzheimer’s disease since the 1970s, given that age-related dementia disorder is also linked to misfolded proteins, along with cell death and connection loss in the brain. Moreover, mice and marmosets develop amyloid plaques when injected with brain fluid containing amyloid-beta proteins.
This new study provides the first hint that a similar transmission event could occur in humans. The aforementioned hormone treatments were extracted and pooled from the pituitary glands of human cadavers, some of which unwittingly carried prions. The original hormone extracts were inaccessible for this study — either due to being tied up in legal cases or misplaced — but the researchers found that amyloid-beta can pass from the brain into pituitary glands in a separate group of Alzheimer’s patients. In other words, it might be possible for amyloid-beta proteins in the brain to taint human growth hormones that are sapped from a cadaver’s pituitary gland.
Does this study mean that Alzheimer’s disease is contagious? The overwhelming response from the researchers and other experts is no.
Here’s why. First, there’s more to Alzheimer’s disease than just amyloid-beta plaques.
“Alzheimer’s disease is a disorder with two features – amyloid deposits called plaques and tau deposits called tangles,” University of Oxford translational neuroscientist Simon Lovestone told Science Media Centre. “There were no tau deposits or tangles in these cases. As it is these lesions or abnormalities that are thought to cause the damage to brain cells and hence the cognitive impairment of dementia, their absence is important and reassuring.”
Interestingly though, tau symptoms tend to occur late in Alzheimer’s disease, and the eight patients in this study died from Creutzfeldt-Jakob disease between the ages of 36 to 51 — long before Alzheimer’s disease usually manifests. None of the patients had the genetic traits for early-onset Alzheimer’s disease.
In other words, even though these patients have amyloid-beta plaques, there is no way to confirm if they had or would have gone on to develop Alzheimer’s disease. As such, the researchers can’t conclude that Alzheimer’s disease is contagious from this single study.
“While these findings are interesting and warrant further investigation, there are too many unknowns in this small, observational study of eight brains to draw any conclusions about whether Alzheimer’s disease can be transmitted this way,” Doug Brown, director of research at Alzheimer’s Society, told Science Media Centre.
“As this research itself states, there is no evidence that Alzheimer’s disease can be transmitted in humans, nor is there any evidence that Alzheimer’s disease can be transmitted through any medical procedure,” said Dame Sally Davies, chief medical officer at the UK Department of Health. All eight patients in this study died and underwent autopsy at the National Hospital in London. Britain has had 65 cases of Creutzfeldt-Jakob linked to these hormone treatments, while France and the U.S. have notched 119 and 29 incidents, respectively.
Collinge echoed the point: “In no way is this [study] suggesting that Alzheimer’s disease is a contagious disease.”
However, Collinge is concerned over whether future investigations might reveals amyloid-beta can spread like prions in iatrogenic Creutzfeldt-Jakob disease.
“We know CJD can be transmitted from person to person through certain medical procedures, not just growth hormone injection. I think it’s worth thinking about whether this might be relevant to other proteins seen in neurodegenerative diseases, such as Alzheimer’s disease,” Collinge said.
Creutzfeldt-Jakob disease comes in different forms. Iatrogenic refers to the kind that is transmitted via medical procedures. Mad Cow disease and its human version, “variant”, is transmitted via food. These are the least common forms. Familial is the hereditary form; sporadic has no known source. These latter two make up the bulk of cases, at 85 percent and 14 percent, respectively. The iatrogenic version is extremely rare.
Howerever, iatrogenic CJD is a major concern because standard hospital sterilization doesn’t completely remove Creutzfeldt-Jakob disease prions from medical instruments. Many hospitals destroy devices exposed to these prions or alternatively use expensive chemical and heat procedures to sterilize them. So if Alzheimer’s disease was found to involve amyloid-beta prions, doctors and hospitals would need to dramatically change how they handle these patients and their biological samples.
But as Lovestone highlights, “Other studies have examined whether there is an increased risk of dementia in people who have had blood transfusion, for example, and there isn’t.” He adds that this hormone treatment was stopped 20 years ago, and there is no evidence from any other paper that the procedure led to amyloid exposure. Following up with more patients who had growth hormone from cadavers more than two decades ago might address this question, he said.
“For the time being, although interesting to researchers, this paper should make us cautious but not overly concerned,” Lovestone said.
Jason Kane contributed to this report.
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