This is a tragic case. In 2015, a paper published in the British journal Nature reported that eight patients had been treated with prion-contaminated cadaveric human growth hormone (c-hGH) and then died of Creutzfeldt-Jakob disease (CJD). The pathological features of amyloid beta were detected in the brain of 4 patients. At the time, c-hGH was considered to be the source of this change. After a lapse of three years, a report published online by Nature on December 13 said that the latest evidence suggests that the patient received cadaveric human growth hormone that is capable of transmitting beta amyloid disease. Iatrogenic infection The iatrogenic human prion disease caused by various medical operations can have an incubation period of more than 50 years. One of the famous cases is the human growth hormone treatment of 1,848 short-skinned people in the UK. The paper published in 2015 pointed out that after receiving human growth hormone treatment contaminated with prions, patients will die from Creutzfeldt-Jakob disease. This is a rare and encephalopathy that has been found to be transmitted. Infected people are usually accompanied by various symptoms such as vision loss, muscle atrophy, progressive dementia, and usually die within one year of onset. People are already familiar with the variant or new variant of the disease - mad cow disease. In this treatment, the human growth hormone used was extracted from the pituitary gland of the corpse, and no one noticed at the time that some of these pituitary glands had been infected with prions. The treatment began in 1958 and stopped in 1985 after a report of Creutzfeldt-Jakob disease occurred in those who received treatment. As of 2000, 38 patients had CJD. But in the gray matter of the brains of these patients with Creutzfeldt-Jakob disease, British scientists unexpectedly discovered the pathological features of amyloid beta. And this time seems to indicate that the patient developed a beta amyloid condition due to c-hGH therapy. Reducing beta amyloid "contamination events" The pathological features of amyloid beta are an important hallmark of cerebral amyloid angiopathy (CAA) and Alzheimer's disease. These patients also have vascular walls that are consistent with Alzheimer's disease and related cerebral amyloid vessels. disease. But these patients who were between the ages of 35 and 51 at the time of death did not have a genetic variant with early-onset Alzheimer's disease. Is it the same as prions, the pituitary gland used to produce human growth hormone, which actually contains the "seed" of amyloid, which leads to the appearance of beta amyloidosis in patients? Further investigation is necessary to determine the source and process of the beta-amyloid "pollution event". In view of this, scientists at the Institute of Prion Diseases at the University College London in the United Kingdom have obtained partial c-hGH samples that have been exposed to patients based on past research. They used biochemical methods to analyze the presence of amyloid beta and tau, and found that several samples were positive. Later, the team studied the beta amyloid in the sample and whether it is possible to spread the beta amyloid pathology in living organisms. The study used genetically engineered mice that expressed the mutant humanized amyloid precursor protein (APP) gene and showed initial signs of beta amyloid deposition at about 6 months of age. Female mice from 6 weeks to 8 weeks old received an intracerebral injection of the original c-hGH sample directly. After 240 days of injection, these mice produced beta amyloid deposition and cerebral amyloid angiopathy, but this was almost completely absent in various control mice (including mice injected with the currently used synthetic recombinant hGH). Does not mean that Alzheimer's disease is an infectious disease This experimental procedure can be summarized as follows: A batch of cadaveric human growth hormone samples were contaminated with amyloid beta, and these samples subsequently developed a phenomenon that can propagate beta amyloid disease in mice. The findings suggest that the original batch of c-hGH contains beta amyloid, which is capable of "seeding" the condition in mice, and experimental evidence also suggests that the human-derived human growth hormone previously received by human patients does indeed transmit beta. Amyloid pathology. The researchers stressed that it is now necessary to test the planting potential of tau in c-hGH samples by a separate mouse model of tau protein. This study does not mean that Alzheimer's disease is an infectious disease or can be transmitted through blood transfusions, but they believe that assessing the risk of iatrogenic transmission of amyloid pathology is important. In other words, this study suggests that people should pay attention to other known iatrogenic routes of transmission, such as the use of surgical instruments, whether they will develop Alzheimer's disease or cerebral amyloid angiopathy. It is related to neurodegenerative diseases. These new findings are not yet able to demonstrate the direct spread of Alzheimer's disease, but support the hypothesis that beta amyloid disease can be transmitted interpersonally through iatrogenic methods. 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