Unearthing Potential Alzheimer's Transmission in Recipients of Discontinued Treatment

29-01-2024
PixelVortex
Unearthing Potential Alzheimer's Transmission in Recipients of Discontinued Treatment
A new study raises new questions about Alzheimer's and other degenerative diseases.
Andrew Brookes/Image Source/Getty Images
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A groundbreaking study published in the journal Nature Medicine has uncovered a potential link between early-onset dementia and a now-discontinued medical treatment involving human growth hormone (HGH). The study suggests that adults who received this treatment as children may be experiencing dementia symptoms due to the transmission of amyloid beta protein, a key component of Alzheimer's disease. While it does not imply that Alzheimer's disease is contagious, the research raises intriguing questions about the transmission and development of degenerative diseases.

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The study explored the cases of five adults who had received pituitary growth hormones prepared from cadavers between 1959 and 1985. These individuals had growth hormone deficiency as children and were part of a group of at least 1,848 people in the UK who underwent this treatment. It was later discontinued when cases of Creutzfeldt-Jakob disease, a rare brain disorder, were found to be associated with the use of contaminated cadaver-derived growth hormone. The researchers found evidence suggesting that the repeated exposure to contaminated HGH may have transmitted Alzheimer's disease through prions and amyloid beta seeds.

Although Alzheimer's disease is not classified as a prion disease, which includes Creutzfeldt-Jakob disease, the study suggests that there are striking similarities. Previous research has shown that the proteins amyloid beta and tau, which are characteristic of Alzheimer's, may behave like prions. The lead author of the study, John Collinge, explained that the findings have implications for the understanding and treatment of Alzheimer's disease, potentially revealing new avenues for therapeutic approaches.

It is important to note that the occurrence of medically acquired Alzheimer's disease through transmission is extremely rare. Dr. Richard Isaacson, who was not involved in the study, emphasized that these findings should not cause fear among the general public. The particular treatment using cadaver-derived growth hormone is no longer in practice, and precautions have been established within modern medical procedures to prevent similar transmissions.

While transmission of Alzheimer's through everyday activities is highly unlikely, the study's findings underscore the importance of reviewing and enhancing sterilization and decontamination measures in medical and surgical procedures. The researchers recommend further investigation to prevent accidental transmissions and ensure patient safety.

Among the eight cases considered in the study, all individuals had a history of receiving human growth hormone derived from cadavers. Five patients experienced symptoms consistent with early-onset dementia, and three of those were diagnosed with Alzheimer's disease. The onset of symptoms occurred between the ages of 48 and 55.

Dr. Gargi Banerjee, the study's first author, highlighted the significance of the research in uncovering the potential transmission of amyloid-beta pathology and its role in Alzheimer's disease. The transmission occurred as a result of treatment with contaminated growth hormone, which involved repeated exposure over several years. Banerjee, however, reiterated that Alzheimer's cannot be acquired through close contact or routine care.

This study is the first of its kind to document the transmission of Alzheimer's disease in humans. Dr. James Galvin, director of the Comprehensive Center for Brain Health at UHealth, University of Miami Health System, believes that further investigation is necessary to better understand the extraneous factors at play in these cases. He points out that while certain proteins involved in brain diseases can be transmitted, such as prion protein in Creutzfeldt-Jakob disease, others like alpha-synuclein in Parkinson's disease and Lewy body dementia do not exhibit the same transmissibility. The study raises intriguing questions about the science of amyloid and tau proteins in Alzheimer's disease, and potential new avenues for research and therapeutic targets.