Early-onset dementia symptoms in five adults may be connected to a now-discontinued human growth hormone medical treatment that they received decades ago as children, a new study suggests.
The study, published Monday in the journal Nature Medicine, provides the first reported evidence of medically acquired Alzheimer’s disease in living people. In these cases, the patients’ early-onset dementia symptoms may be the result of the possible transmission of amyloid beta protein, which is a key component of Alzheimer’s disease when it forms plaques in the brain.
Abnormal buildup of the protein amyloid beta in the brain is associated with Alzheimer’s and the new study suggests that amyloid beta contamination may have a connection with the early dementia symptoms experienced by the patients in the study. The study findings do not suggest that Alzheimer’s disease can be contagious, or spread like viral or bacterial infections, for instance, but they raise new questions about Alzheimer’s and other degenerative diseases.
“I should emphasize these are very rare occurrences, and the majority of this relates to medical procedures that are no longer used,” John Collinge, lead author of the study and director of the University College London Institute of Prion Diseases, said in a news briefing.
All five adults had growth hormone deficiency as children and received pituitary growth hormones prepared in a specific way from cadavers. The pituitary gland is located at the base of the brain, and human growth hormone, or HGH, is a natural hormone the gland makes and releases, promoting growth in children.
Between 1959 and 1985, these patients were among the at least 1,848 people in the United Kingdom who were treated with a human growth hormone derived from a cadaver’s pituitary gland, according to the study. At the time, this treatment also was used in other parts of the world, including the United States. The treatment approach was discontinued after cases of a rare brain disorder called Creutzfeldt-Jakob disease were found to be associated with the administration of contaminated human growth hormone from cadavers.
The new study suggests that repeated exposure, over multiple years, to treatments with cadaver-derived HGH that had been contaminated by both prions associated with Creutzfeldt–Jakob disease and amyloid beta seeds could transmit Alzheimer’s disease. Prions are proteins that can act as transmissible agents of neurodegenerative diseases.
The researchers wrote in their study that Alzheimer’s disease may be transmissible, in certain circumstances, in a way similar to conditions known as “prion diseases” — a family of rare progressive neurodegenerative disorders known to be associated with prion proteins, including Creutzfeldt–Jakob disease or CJD. Although Alzheimer’s is not a prion disease, some separate research suggests that the two proteins that are hallmarks in Alzheimer’s disease — amyloid beta and tau — behave like prions.
“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,” Collinge said in the news briefing. “It does raise implications about therapeutic approaches to Alzheimer’s disease.”
