A team of scientists from University College London have reported the first clear evidence of human-to-human transmission of Alzheimer’s disease in a new study.
A team of researchers from University College London has reported the first clear evidence of human-to-human transmission of Alzheimer’s disease. In a handful of extraordinarily rare case studies, the researchers showed how human growth hormone treatment transfers toxic proteins to children and causes early-onset Alzheimer’s development.
“Can Alzheimer’s be transmitted from person to person?”
In 1,800-odd cases over nearly 25 years from the late 1950s, human growth hormone was used sporadically to treat children with certain physical developmental problems. The hormone, known as C-hGH (cadaver-derived human growth hormone), was harvested from the pituitary glands of deceased people and injected into unusually short children. Over the years, an unexpectedly high percentage of children treated with growth hormone developed a fatal neurodegenerative condition called Creutzfeldt-Jakob disease. This disease was caused by toxic misfolded proteins called prions. Researchers discovered that some samples of c-hGH contained toxic prions, sowing the seeds of the neurodegenerative disease in healthy brains. Human-derived growth hormone was quickly replaced with a safer, synthetic version.
More recently, a team of researchers studying brain tissue samples from growth hormone patients who died from Creutzfeldt-Jakob disease discovered interesting signs of Alzheimer’s disease. The deceased patients harbored an unusually high accumulation of amyloid proteins, a hallmark of Alzheimer’s disease. This raised the question: Can Alzheimer’s be transmitted from person to person, as is the case with other prion diseases?
The hypothesis of human-to-human transmission of Alzheimer’s disease was starting to sound plausible, but researchers still needed some kind of hard evidence.
First evidence that Alzheimer’s is contagious
The research team examined eight patients who had recently presented with neurological problems at the National Prion Clinic in London. All eight patients had been treated with c-hGH in childhood and were now aged between 38 and 55. Five of these patients had been diagnosed with early-onset dementia but had no pathologic signs of Creutzfeldt-Jakob disease. All five of these patients met the diagnostic criteria for Alzheimer’s but, importantly, showed no evidence of a genetic predisposition to early onset of the disease.
Andrew Doig from the University of Manchester says the new findings are comprehensive and cautionary, but warns against drawing broader conclusions based on just eight rare cases. “While the new type of Alzheimer’s reported here is of great scientific interest because it reveals a new way the disease spreads, there is no reason to fear it as the pathway was halted 40 years ago,” says Doig, who was not involved in the new research.
While these findings represent an extraordinarily rare example of human-to-human transmission of Alzheimer’s, the chances of such a case happening today are extremely low. But the research team’s discovery could provide new insights into how the disease progresses and lead to new treatments.
