A team from University College London has reported the first clear evidence of human-to-human transmission of Alzheimer's disease. A research team reports that at least five cases of Alzheimer's disease are believed to be due to medical treatments from decades ago.
Using unusually rare cases, researchers have shown how treatment with human growth hormone can transplant toxic proteins into children and lead to the development of early-onset Alzheimer's disease.

For about 25 years, starting in the late 1950s, human growth hormone was used sporadically to treat children with certain physical developmental problems. The hormone, called "c-hGH" (cadaveric human growth hormone), was extracted from the pituitary glands of deceased people and injected into children of unusually short stature.

Over the years, an unexpectedly high proportion of children treated with growth hormone developed Creutzfeldt-Jakob disease, a fatal neurodegenerative disease. The disease is caused by toxic misfolded proteins called prions. By 1985, there was conclusive evidence linking growth hormone to Creutzfeldt-Jakob disease. Researchers found that some growth hormone samples contained toxic prions, which sow the seeds of neurodegenerative disease in healthy brains. Growth hormone of human origin was quickly replaced by safer synthetic hormones.

Recently, a team of researchers discovered strange signs of Alzheimer's disease while studying brain tissue samples from growth hormone patients who died from Creutzfeldt-Jakob disease. These deceased patients had abnormally high levels of amyloid deposits, a tell-tale sign of Alzheimer's disease. So, a question arises: Can Alzheimer's spread from person to person like other prion diseases?

Because the time it took for these patients to die from Creutzfeldt-Jakob disease was too short, it was impossible to tell whether they would develop Alzheimer's. However, a subsequent study did find that some c-hGH samples contained accumulation of amyloid, and animal tests showed that mice injected with contaminated growth hormone developed pathological signs of Alzheimer's disease.

So at this point, the hypothesis that Alzheimer's disease spreads from person to person is credible, but researchers still need some kind of hard evidence. To do this, the team investigated eight patients with neurological disorders who had recently been referred to the National Prion Clinic in London. All eight patients received c-hGH treatment during childhood and are now aged between 38 and 55 years old.

Five of the patients were diagnosed with dementia praecox but had no pathological signs of Creutzfeldt-Jakob disease. All five patients met diagnostic criteria for Alzheimer's disease but, importantly, showed no genetic predisposition to early-onset dementia.

"Here, we describe recipients who develop dementia and biomarker changes within the AD phenotypic spectrum, suggesting that AD, like CJD, has environmentally acquired (congenital) forms as well as late-onset sporadic and early-onset hereditary forms," ​​the researchers wrote in their newly published study. "While congenital AD may be rare and there is no indication that Aβ [amyloid-β] is transmitted from person to person during activities of daily living, recognition of it underscores the need to revisit measures to prevent accidental transmission through other medical and surgical procedures."

Andrew Doig of the University of Manchester said the new findings were comprehensive and careful, but cautioned against making broader extrapolations from what was essentially just eight very rare cases.

"While the new form of Alzheimer's reported here is of great scientific interest because it reveals a new way in which the disease is transmitted, there is no reason to be afraid because the disease's causative mode was stopped more than 40 years ago. Transmission of disease between human brains in this way will never happen again," Doig said.

Susan Kohlhaas of Alzheimer's Research UK agreed, saying the findings did demonstrate an unusually rare instance of Alzheimer's spreading from person to person, but noted that such cases were unlikely to occur today. Instead, Kohlhaas said, the discovery is expected to provide researchers with new insights into how the disease develops, helping them find new treatments.

"There is no evidence that amyloid can be spread through any other route, such as everyday activities or routine medical procedures," Kohlhaas said. "But this study reveals more about how amyloid fragments spread within the brain, providing further clues into how Alzheimer's develops and potential new targets for future treatments."

The new research is published in the journal Nature Medicine.