Health UK (Commonwealth Union) – Researchers focused on Alzheimer’s diseases from across the world have long been focused on halting the activities of amyloid-beta as it is believed to play a key role in the disease. Alzheimer’s diseases together with many other neurological conditions such as Parkinsons disease and ALS are also a key focus for anti-ageing researchers as they represent a large obstacle to healthy ageing.
A team of researchers from UCL and UCLH have reported that five cases of Alzheimer’s disease are suspected to have originated from medical treatments administered decades earlier.
Researchers of the study point out that Alzheimer’s disease, typically occurring in late adulthood as a sporadic condition or, less commonly, as an inherited disorder linked to a faulty gene, is triggered by the amyloid-beta protein. This recent study published in Nature Medicine presents the initial evidence of Alzheimer’s disease in living individuals that seems to have been acquired through medical means, specifically the transmission of the amyloid-beta protein.
The individuals discussed in the study were all subjected to childhood treatment involving a form of human growth hormone derived from cadaver pituitary glands (referred to as cadaver-derived human growth hormone or c-hGH). This treatment was administered to at least 1,848 individuals in the UK between 1959 and 1985 to address various causes of short stature. The usage of c-hGH was discontinued in 1985 after it was discovered that certain batches were contaminated with prions, infectious proteins responsible for causing Creutzfeldt-Jakob disease (CJD), in some recipients. Synthetic growth hormone, devoid of the risk of transmitting CJD, replaced c-hGH thereafter.
Earlier research by these scientists indicated that individuals who contracted CJD as a result of c-hGH treatment (referred to as iatrogenic CJD) exhibited premature accumulation of amyloid-beta protein in their brains. In a 2018 study, the researchers demonstrated that archived samples of c-hGH were contaminated with amyloid-beta protein and, even after decades of storage, were capable of transmitting amyloid-beta pathology to laboratory mice upon injection. This led them to speculate that individuals exposed to contaminated c-hGH, who did not develop CJD and lived longer, might eventually manifest Alzheimer’s disease.
The most recent study focuses on eight individuals who were referred to UCLH’s National Prion Clinic at the National Hospital for Neurology and Neurosurgery in London, all of whom had received c-hGH treatment during childhood, often spanning several years.
Among these individuals, five exhibited symptoms of dementia, either having been previously diagnosed with Alzheimer’s disease or meeting the diagnostic criteria for it; one person displayed criteria for mild cognitive impairment. Onset of neurological symptoms occurred between the ages of 38 and 55 for this group. Biomarker analyses supported Alzheimer’s disease diagnoses in two patients, while indicating potential Alzheimer’s in another; autopsy findings confirmed Alzheimer’s pathology in a separate patient.
The remarkably early onset of symptoms suggests a departure from typical sporadic Alzheimer’s, which is typically associated with advanced age. Genetic testing ruled out inherited Alzheimer’s disease in the five patients for whom samples were available.
Since c-hGH treatment is no longer administered, there is no risk of new transmission through this avenue. Additionally, there have been no documented instances of Alzheimer’s transmission via other medical or surgical procedures. It is not implied that amyloid-beta can be transmitted in everyday life or through routine medical or social care practices, according to the researchers of the study.
Nevertheless, the researchers emphasize the significance of reassessing precautions to mitigate any potential inadvertent transmission of amyloid-beta through other medical or surgical procedures, particularly those previously associated with accidental transmission of CJD.
Professor John Collinge, Director of the UCL Institute of Prion Diseases and a consultant neurologist at UCLH, who is the lead author for the research, says “There is no suggestion whatsoever that Alzheimer’s disease can be transmitted between individuals during activities of daily life or routine medical care. The patients we have described were given a specific and long-discontinued medical treatment which involved injecting patients with material now known to have been contaminated with disease-related proteins.
“However, the recognition of transmission of amyloid-beta pathology in these rare situations should lead us to review measures to prevent accidental transmission via other medical or surgical procedures, in order to prevent such cases occurring in future.
“Importantly, our findings also suggest that Alzheimer’s and some other neurological conditions share similar disease processes to CJD, and this may have important implications for understanding and treating Alzheimer’s disease in the future.”
