Alzheimer’s disease, a devastating neurological condition affecting people in late adulthood, may have been acquired by five individuals through medical treatments received decades ago. This marks the first instance of Alzheimer’s in living patients potentially linked to medical procedures.
Alzheimer’s and a discontinued childhood medical treatment
The individuals in question were treated as children with cadaver-derived human growth hormone (c-hGH), extracted from the pituitary glands of deceased donors. This treatment was administered to at least 1,848 people in the UK between 1959 and 1985 for various forms of short stature. The practice was discontinued in 1985 after it was discovered that some batches of c-hGH were contaminated with infectious proteins called prions, responsible for Creutzfeldt-Jakob disease (CJD) in some patients. Fortunately, this medication was replaced a long time ago by synthetic growth hormone, which is free from the risk of transmitting CJD.
The same researchers previously found that some patients with CJD due to c-hGH treatment had also developed deposits of amyloid-beta protein in their brains prematurely. Further research in 2018 revealed that archived samples of c-hGH were contaminated with amyloid-beta protein. When injected into laboratory mice, these samples transmitted amyloid-beta pathology, suggesting that long-term survivors of c-hGH treatment might develop Alzheimer’s disease.
Amyloid-beta, a fragment produced from a larger precursor protein, is now considered a hallmark of Alzheimer’s. Patients with this condition have unusually high quantities of amyloid-beta in their brains.
In a healthy brain, amyloid-beta plays various roles, including regulating neural activity and supporting brain health. However, in Alzheimer’s disease, something goes awry. The protein begins to accumulate, forming clumps and eventually dense, insoluble plaques that disrupt brain function. This process is believed to be a critical factor in the onset and progression of Alzheimer’s, but the exact reasons why and how this accumulation occurs remain one of the great mysteries of modern neuroscience.
An unfortunate finding
The new study focuses on eight individuals who received c-hGH treatment in childhood. The patients were admitted to the University College London’s National Prion Clinic at the National Hospital for Neurology and Neurosurgery. Among them, five displayed dementia symptoms consistent with Alzheimer’s disease or met the diagnostic criteria for it.
What is striking is their age range: 38 to 55 years when symptoms appeared, far younger than the typical onset age for sporadic Alzheimer’s in the mid-60s or later. Genetic testing ruled out inherited Alzheimer’s in these patients.
The c-hGH treatment is now obsolete, so there is no risk of new transmissions via this route. The authors of the study emphasize that the circumstances of these Alzheimer’s cases are highly unusual and that the disease cannot be spread through daily contact. There is no way you can get Alzheimer’s through close contact or routine care of a patient — that was never a remote possibility.
However, now that this old treatment has been strongly linked to acquired Alzheimer’s, one can only wonder if other treatments, discontinued or otherwise, may also be responsible for Alzheimer’s.
“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, to prevent such cases from occurring in the future,” said lead author Professor John Collinge, Director of the UCL Institute of Prion Diseases.
“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.”
The findings appeared in the journal Nature Medicine.
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