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The Curious Link Between Alzheimer’s and Cadaver-Derived Growth Hormones

Researchers have identified the first cases of Alzheimer's being transmitted between humans, shedding light on the disease's mechanisms. Eight patients, five alive, acquired the disease through a now-banned medical procedure involving cadaveric growth hormone. This procedure unintentionally transmitted amyloid beta, a key Alzheimer's protein. The findings suggest similarities between Alzheimer's and prion diseases like Creutzfeldt-Jakob. Despite lacking genetic risk factors, all patients shared the HGH treatment, prompting further inquiry into Alzheimer's elusive origins.

Staff Editor February 13, 2024

In a groundbreaking study published in the prestigious journal Nature Medicine, a group of researchers have revealed a shocking discovery – the first-ever cases of Alzheimer’s disease being transmitted between humans. While the occurrences were extremely rare and unusual, they offer valuable insights into the mechanisms underlying this devastating disease.

The study details how eight adult patients, five of whom are still alive, likely contracted Alzheimer’s through a banned medical procedure in which they were given human growth hormone extracted from a cadaver’s brain during childhood. This procedure inadvertently transmitted a protein called amyloid beta, which is believed to play a central role in the development of Alzheimer’s disease.

Lead author of the study, John Collinge, the director of the University College London Institute of Prion Diseases, highlighted the rarity of such cases, emphasizing that the medical procedures responsible for the transmission are no longer in use. The use of cadaver growth hormones, now synthesized, was banned in the 1980s due to its link to Creutzfeldt-Jakob disease (CJD), a fatal brain disorder caused by misfolded proteins called prions.

The researchers’ findings suggest a striking similarity between the transmission of beta-amyloids in Alzheimer’s disease and prion diseases like CJD, which have long been known to pass between humans. The abnormal aggregates of misfolded proteins in Alzheimer’s appear to propagate in a manner akin to human prion diseases.

One notable aspect of the study is that none of the patients showed genetic mutations associated with early-onset dementia, despite experiencing symptoms at a young age. Only one patient had genetic markers for late-onset dementia. Interestingly, none of the patients exhibited elevated levels of tau protein, commonly linked to cognitive decline, highlighting the unique nature of their condition.

The common thread among the patients was the shared history of receiving the HGH procedure, prompting important questions about the nature of Alzheimer’s disease. This discovery challenges existing notions about the disease and underscores the need for further research to unravel its complexities.

In conclusion, the study sheds new light on the potential modes of transmission of Alzheimer’s disease and offers a fresh perspective on its origins. While the cases observed are indeed rare, they provide a critical foundation for understanding Alzheimer’s and advancing efforts towards effective prevention and treatment strategies.