A study published Wednesday in the journal Nature by British researchers John Collinge and Sebastian Brandner provides stunning evidence that Alzheimer's disease may be transmissible to humans through certain medical or surgical procedures.

It involved autopsies of eight British patients, ages 36 to 51, who are believed to have come down with Creutzfeldt-Jakob disease (CJD) through treatment with human growth hormone from cadavers. In addition to evidence of CJD, analysis of their brain tissue samples revealed a second worrisome abnormality.

Six of the individuals had some degree of precursors for something called beta amyloid -- the abnormal protein that forms a main component of the plaques found in the brains of patients with the disease. That's very unusual in this relatively young age range. This phenomenon may have been due by genetic mutations associated with early-onset Alzheimer's, but none of them had those either.

The explanation that was left: Could it be that the human growth hormone treatment also transmitted something related to Alzheimer's?

Here's what you need to know about the research:

What is the main takeaway from the study?

That healthy individuals exposed to cadaver-derived human growth hormone may be at risk of these conditions as they age. Researchers said further research needs to be done to understand what mechanisms may be involved but that it "seems likely" that prions and pituitary glands used to make the human growth hormone contained the "amyloid beta seeds" that caused the amyloid beta abnormalities observed.

Does this mean Alzheimer's is contagious?

No, not in the way you're probably thinking.

There's no evidence in this study that Alzheimer's (or cerebral amyloid angiopathy, a related neurological condition) can be spread from person to person by direct contact. Researchers Mathias Jucker, of the Hertie Institute for Clinical Brain Research at the University of Tübingen, and Lary C. Walker, of the Center for Neurodegenerative Disease at Emory University, emphasized in a commentary accompanying the Nature study that "so far, there is no indication that Alzheimer’s disease can be transmitted between people under ordinary circumstances."

However, the study does provide some strong evidence that precursors for beta amyloid which is found in Alzheimer's patients' brains could be transmitted via certain medical procedures.

Can you back up and tell me more about what happened in the past with the patients treated with human growth hormone (HGH)?

The researchers in the Nature study drew parallels between what they found and previous findings that diseases caused by prions could be transmitted as a result of some medical procedures.

One of the most well-documented cases involved people in Britain who were treated in 1958-1985 with human growth hormone that was extracted from pituitary glands of cadavers that were prion-contaminated and who developed Creutzfeldt–Jakob disease. As of 2012, 450 cases of Creutzfeldt–Jakob disease have been documented to be linked to cadaver-derived HGH and to a lesser extent other medical procedures including transplant and neurosurgery.

It's important to note that the incubation period appears to be very long, 30 or even 50 years in these cases.

What are some limitations of the new research?

First, it's a very small sample. Second, the study found that the precursors for beta amyloid might be transmissible but there's no information to make the leap -- a pretty big one -- to conclude that that would have lead to Alzheimer's in those individuals or others.

I'm still concerned. Does this mean I should avoid medical procedures? What about dental procedures or blood transfusions?

In a statement, study author Collinge, of University College London, emphasized that the findings "relate to the specific circumstance of cadaver-derived human growth hormone injections, a treatment that was discontinued many years ago."

"It is possible our findings might be relevant to some other medical or surgical procedures, but evaluating what risk, if any, there might be requires much further research," he said. "Our current data have no bearing on dental surgery and certainly do not argue that dentistry poses a risk of Alzheimer’s disease.”

Health researchers also say there's no reason to worry about blood transfusions at this time.

What do other experts have to say about the study?

John Hardy, molecular neuroscientist, University College London:

“This is the first evidence of real-world transmission of amyloid pathology. It is potentially concerning.”

Sally Davies, chief medical officer, United Kingdom Department of Health:

“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. This was a small study on only eight samples. We monitor research closely and there is a large research programme in place to help us understand and respond to the challenges of Alzheimer’s. I can reassure people that the [National Health Service] has extremely stringent procedures in place to minimise infection risk from surgical equipment, and patients are very well protected.”
--United Kingdom Department of Health

Roger Morris, professor of molecular neurobiology, King’s College London:

“Does this Nature paper, from the London labs of John Collinge and Sebastian Brandner, presage a new era in which Alzheimer’s disease changes from being an isolated disease of each individual as they age, to becoming infectious and able to attack everyone, young and old? No.
This is a landmark paper in providing evidence, for the first time in man, of a mechanism for the propagation of Alzheimer’s disease that we already know exists from experimental studies in mice: the amyloid fibrils formed in the brains of Alzheimer’s patients, if injected into normal brain, infect the host brain...
Arguably the most important point of this paper is to provide observational evidence in man, adding to the growing weight of experimental evidence in mice, that Alzheimer’s, the most common neurodegenerative disease, shares mechanistic features with CJD."
--Science Media Centre

Are there other studies about this issue? What do they show?

Perhaps the most highly publicized studies on this subject came out in 2011 and 2012. One study, by Claudio Soto, a professor of neurology at the University of Texas Medical Center and published in Molecular Psychiatry, was a preliminary "proof of concept" study. It involved injecting mice with tissue from a human with Alzheimer's and they found that the mice exhibited changes characteristic of the disease.

The second was published in PLoS One and suggested that one of the abnormalities that leads to the disease may spread like a virus from nerve cell to nerve cell. The work involved a genetically engineered mouse strain that carries the human version of the gene for tau, which is one of the main proteins that builds up in the brains of Alzheimer's patients.

"We designed the experiments to tell if the cell is up regulating its own production of tau, as a result of being in the same environment of the cells making human tao," Karen Duff, a professor at Columbia University and lead author of the paper told Time. "And we came to the conclusion that the tau was spreading. We suspect that the original cell dies and the tau is picked up by neighboring cells."

A third study published in 2013 in JAMA Neurology involved analyzing data from 6,190 people who had growth issues and received injections of human growth hormones taken from cadavers. In inspecting death certificates from those who had died they found no mention of Alzheimer's (or Parkinson's for that matter.) At the time, John Trojanowski, the senior author, told Fox News that it should be "reassuring" to people who had transplants, blood transfusions and the like.

This work doesn't contradict the study out this week since the eight people whose brain tissue was analyzed did not have symptoms of Alzheimer's and died of other causes that would be listed on their death certificates. The big question raised by the Nature study, of course, is whether they may have been at higher risk of developing the disease had they lived longer.

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