A new study has identified a potential link between a discontinued growth hormone treatment and early-onset Alzheimer’s disease.
Researchers from University College London examined cases of patients who developed Alzheimer’s in their 30s, 40s and 50s after receiving cadaver-derived growth hormone injections as children. This growth hormone, known as c-hGH, was suspended in 1985 when it was found to transmit Creutzfeldt-Jakob disease in some patients.
Of eight former c-hGH recipients studied, five showed signs of amyloid protein buildup in the brain and met the diagnostic criteria for Alzheimer’s – an unusually early age for such symptoms. Genetic testing confirmed their disease was not inherited.
“We have found that it is possible for amyloid-beta pathology to be transmitted and contribute to the development of Alzheimer’s disease,” said lead researcher Dr. Gargi Banerjee in a press release. “This transmission occurred following treatment with a now-obsolete form of growth hormone, and involved repeated treatments with contaminated material, often over several years.”
The study authors emphasized Alzheimer’s cannot be spread through routine daily contact or medical procedures.
“There is no suggestion whatsoever that Alzheimer’s disease can be transmitted between individuals during activities of daily life or routine medical care,” said senior author Professor John Collinge, director of the UCL Institute of Prion Diseases.
Rather, the early Alzheimer’s cases appear linked to injections of growth hormone containing proteins associated with neurodegenerative disorders. This type of cross-infection is extremely rare.
Still, researchers say the findings highlight the need to safeguard against accidental transmission of proteins that could trigger brain disease. They recommend investigating any other outdated medical treatments that might harbor similar risks.
Understanding Early-Onset Alzheimer’s
While Alzheimer’s overwhelmingly strikes older adults, an early-onset form of the disease affects those younger than 65. Most early-onset Alzheimer’s cases are attributed to gene mutations.
The newly identified growth hormone link provides clues into a very small subset of early-onset Alzheimer’s not caused by genetics.
“The study describes just five Alzheimer’s patients out of the more than 1,800 people who were known to have received growth hormone in this way,” noted Dr. Rehan Aziz, a psychiatrist not involved with the research. “The unusually young age at which these patients developed symptoms suggested they did not have the usual form of Alzheimer’s associated with old age.”
The Role of Amyloid Proteins
Amyloid beta proteins form harmful clumps and plaques in the brains of those with Alzheimer’s disease. The new study proposes that certain medical procedures may be able to transmit these proteins in a prion-like manner.
Prions are misfolded proteins that can induce normal proteins around them to also take an abnormal shape. This self-propagating process leads to prion diseases like Creutzfeldt-Jakob.
Researchers speculate that growth hormone derived from cadavers may have initiated a similar self-propagation of amyloid beta, eventually causing Alzheimer’s pathology. But this type of transmission requires direct injection of contaminated material into the body.
“The research raises the question of whether beta-amyloid protein can propagate itself, leading to cascading memory loss and worsening Alzheimer’s pathology,” said Dr. Aziz.
Alzheimer’s Isn’t Contagious
While the study uncovered a very rare mechanism of Alzheimer’s transmission, experts underscore that Alzheimer’s is not contagious through everyday interactions.
“You can’t catch Alzheimer’s by taking care of someone with Alzheimer’s,” said Christopher Weber, PhD of the Alzheimer’s Association. “Alzheimer’s disease is not transmissible through the air, or by touching or being near someone with Alzheimer’s.”
Routine medical care also does not pose a risk. “These findings should not cause concern for patients and their families,” Weber added.
Researchers recognize the study’s limitations, including an extremely small sample size. More work is needed to confirm this novel concept of a “transmissible” Alzheimer’s subtype.
But if validated, the findings could help guide medical protocols to avoid the spread of disease-causing proteins through contaminated injections or procedures. While highly uncommon, similar transmission is theoretically possible if safeguards aren’t in place.
“We shouldn’t put amyloid-beta into people’s brains, either accidentally or on purpose,” said Weber, underscoring the importance of eliminating any pathogen transmission risks associated with certain treatments.