New Study Links Alzheimer’s Disease to Past Medical Procedures, Raises Questions about Rare Transmission
In a groundbreaking study published in Nature Medicine, researchers from the University College London (UCL) have identified a potential link between Alzheimer's disease and specific medical treatments administered decades ago. While Alzheimer's has traditionally been associated with internal factors such as age, family history, lifestyle choices, and certain medical conditions, this research highlights cases where the disease may have been triggered by a particular medical intervention.
The focus of the study was on patients who had received human growth hormone treatments, specifically a type extracted from the pituitary glands of deceased individuals (c-hGH). The researchers discovered that this particular form of growth hormone was associated with increased levels of amyloid-beta protein in the brain, a key factor in Alzheimer's development. Among the eight individuals studied who had been treated with c-hGH as children, five later developed symptoms of dementia, meeting the criteria for Alzheimer's disease. Notably, all these patients began experiencing cognitive decline between the ages of 38 and 55.
Dr. Gargi Banerjee, the first author of the study, emphasized that the transmission of amyloid-beta pathology leading to Alzheimer's occurred due to the administration of a now-obsolete form of growth hormone. This transmission involved repeated treatments with contaminated material over several years, primarily before the suspension of this growth hormone treatment in 1985 due to its association with Creutzfeldt-Jakob disease (CJD), a degenerative brain disorder causing dementia and death.
The study's lead author, Professor John Collinge, stressed that Alzheimer's disease is not contagious through routine daily activities or common medical care. The patients in the study received a specific and discontinued treatment that involved injecting contaminated material.
Although the study suggests a potentially rare and transmissible form of Alzheimer's, Dr. Rehan Aziz, a geriatric psychiatrist, noted the limited scope of the research, covering only five patients out of over 1,800 who received similar growth hormone treatments. The unusually young age at which these patients developed symptoms raises questions about whether the beta-amyloid protein can propagate itself, contributing to early-onset Alzheimer's pathology.
Christopher Weber, PhD, director of global science initiatives at the Alzheimer's Association, underscored the non-contagious nature of Alzheimer's and highlighted the study's limitations, urging the need for replication and confirmation to establish the credibility of a possible 'rare acquired' Alzheimer's type.
Weber emphasized the importance of understanding potential risks and ensuring the elimination of all methods of pathogen transmission, even if the identified transmission of amyloid-beta is rare. He stressed the need for vigilant measures, such as the complete sterilization of surgical instruments, to prevent the inadvertent introduction of amyloid-beta into individuals' brains.
In conclusion, while this study sheds light on an unusual transmission of amyloid-beta leading to Alzheimer's, it underscores the extraordinary nature of these occurrences and the need for ongoing research to confirm and further understand the findings. The scientific and clinical communities must remain vigilant in implementing measures to prevent any inadvertent transmission of disease-related proteins in medical procedures.