One of the main causes of Alzheimer’s disease is the accumulation of a pathogenic form of beta-amyloid protein in the brain. Typically, the disease occurs sporadically due to the accumulation of mutations towards the end of adult life or, less commonly, due to an inherited defective gene. In a new article published in the magazine Nature Medicine, presented cases of Alzheimer’s disease acquired after medical intervention long before the first manifestations of the disease and caused by the transmission of a pathogenic form of beta-amyloid protein.
All the patients described in the article, as children, received human growth hormone isolated from the pituitary gland of deceased people. This method was used to treat various causes of short stature in at least 1,848 people in the UK from 1959 to 1985. It was later abandoned when it was discovered that some batches of such hormones were contaminated with defective prions (abnormal proteins twisted into a pathogenic shape) that caused the fatal prion disease Creutzfeldt-Jakob disease. Subsequently, growth hormone from dead people was replaced with a synthetic analogue that does not carry the risk of transmitting pathogenic forms of prions.
In earlier work, scientists reported that some patients with Creutzfeldt-Jakob disease, which resulted from treatment with cadaveric growth hormone, prematurely developed deposits of beta-amyloid protein in the brain. Also in another paper, the authors showed that archival samples of growth hormone from dead people contaminated with beta-amyloid protein, even decades later, transmitted beta-amyloid pathology to laboratory mice when it was administered. Therefore, scientists hypothesized that people exposed to the contaminated hormone who did not develop Creutzfeldt-Jakob disease and lived longer might eventually develop Alzheimer’s disease.
The authors of the new paper reported on eight people who were treated with cadaveric growth hormone during childhood, often over several years. Five of them had symptoms of dementia with already diagnosed Alzheimer’s disease or meeting the diagnostic criteria for this condition. One additional patient met the criteria for mild cognitive impairment. All were between 38 and 55 years old when neurological symptoms appeared. Biomarker analysis confirmed the diagnosis of Alzheimer’s disease in two people and also predicted the onset of the disease in another. In another case, the presence of Alzheimer’s disease was confirmed by a post-mortem autopsy.
The unusually young age at which these patients began developing symptoms, coupled with the fact that they had been treated with growth hormone from dead people during childhood, suggested that they did not have the usual sporadic Alzheimer’s disease that often occurs as modern people age. The team also ruled out hereditary Alzheimer’s disease in five patients whose samples were available for genetic testing. All this supported the conclusion: the cause of Alzheimer’s disease in the described cases is the transmission of a pathogenic form of beta-amyloid during treatment in childhood.
The circumstances under which these people tragically developed Alzheimer’s disease are extremely unusual. Since growth hormone treatment of dead people is no longer practiced, there is no risk of any new transmission through this route. There are no reported cases of Alzheimer’s disease acquired as a result of any other medical or surgical procedure. There is also no suggestion that beta-amyloid can be transmitted in everyday life or during routine medical or social care.
The results showed that Alzheimer’s disease and some related neurological diseases share pathological processes with Creutzfeldt-Jakob disease. This may prompt the development of new treatment strategies for dementias associated with pathological forms of beta-amyloid protein.
2024-01-29 16:01:17
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