Can Alzheimer's be transmitted between people?

According to a January study published in Nature Medicine, some patients who received a growth hormone treatment between the late 1950s and the mid-1980s later went on to develop Alzheimer's disease.

Between 1959 and 1985, at least 1848 patients in the United Kingdom received human growth hormone that was taken from a cadaver's pituitary gland. At the time, donated growth hormone was used as a treatment in several countries, including the United States and Australia.

However, the practice was ended after 200 patients worldwide developed Creutzfeldt-Jakob disease (CJD), a rare and fatal brain disorder caused by infectious proteins called prions, after receiving contaminated growth hormone from the cadaver.

In 2015, researchers suggested that there was "possible evidence" that amyloid beta protein, which is associated with Alzheimer's, could have been transmitted from the cadaver growth hormone. The researchers later administered the cadaver hormone to mice and found that they developed amyloid-beta plaques in their brains.

This finding, according to researchers, suggested that patients who received the contaminated growth hormone may have also received misfolded amyloid-beta proteins, which could have led them to eventually develop Alzheimer's.

After evaluating eight patients from the U.K. cohort, five were found to have developed Alzheimer's — and at unusually young ages. The patients began developing symptoms between the ages of 38 and 55, and genetic sequencing did not reveal any mutations that would increase their risk of the disease.

"This study suggests that in very rare circumstances Alzheimer's disease may be transmitted between humans via human growth hormone from deceased donors. It must be stressed that this treatment is no longer used today and has been replaced with synthetic growth hormone," said Susan Kohlhaas, executive director of research and partnerships at Alzheimer's Research U.K. "It's also important to stress that this is the only recorded instance of Alzheimer's transmission between humans."

In a separate study recently published in Stem Cell Reports, researchers bred mice to carry a human version of the amyloid precursor protein gene variant. The mice with the mutated gene all developed an Alzheimer's-like disease.

After extracting bone marrow from these mice, the researchers transplanted it into two healthy groups of mice. One group did not have the amyloid precursor gene at all, and the second group had a normal mouse version of the gene.

Both healthy mice groups eventually began showing signs of Alzheimer's after receiving the bone marrow. Symptoms of cognitive decline were observed at both a behavioral and molecular level, with the mice having increased formation of amyloid plaques and a leaky blood-brain barrier.

According to the researchers, the findings suggest the donor cells containing the mutation caused Alzheimer's disease in the healthy mice.

Commentary

Even with these findings, researchers emphasize that Alzheimer's is not an infectious disease and cannot be transmitted from person to person like the common cold.

"There is no suggestion whatsoever that Alzheimer's disease can be transmitted between individuals during activities of daily life or routine medical care," said John Collinge, director of the UCL Institute of Prion Diseases and the senior author of the first study.

"… However, the implications of this paper we think are broader with respect to disease mechanisms — that it looks like what's going on in Alzheimer's disease is very similar in many respects to what happens in the human prion diseases like CJD, with the propagation of these abnormal aggregates of misfolded proteins and misshapen proteins," Collinge said.

Outside researchers also noted that some of the findings of the first study were unclear, especially since there was limited information available from the affected patients.

"Can the pathology be transmitted? Yes, it can, and that's important conceptually," said Ben Wolozin, an expert on neurodegenerative diseases at Boston University's medical school. "The question is, what's driving disease? There are many weird things about these rare cases. What's unclear from the images is, why would they develop such severe dementia that quickly?"

Going forward, more research is likely to be needed to better understand the potential causes of Alzheimer's.

"I would say at this point, there is nothing additional that we need to do as far as clinical practice, but this certainly lends itself to asking new scientific questions," said James Galvin, director of the Comprehensive Center for Brain Health at the University of Miami Health System.

"Proteins involved in brain disease, such as prion protein in Creutzfeldt-Jakob disease and bovine spongiform encephalopathy, are transmissible," Galvin continued. "Additionally, other proteins involved in disease, such as alpha-synuclein in Parkinson's disease and Lewy body dementia, share some of these properties but do not appear to be transmissible. The science of amyloid and tau proteins in Alzheimer's disease may need to be revisited." (Joseph, STAT, 1/29; Prater, Fortune, 2/1; Howard, CNN, 1/29; Macfarlane, The Conversation, 2/1; Haseltine, Forbes, 4/9)

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