A Breakthrough in Alzheimer’s Research

Medical science has shown remarkable progress in recent decades. Scientists, biomedical engineers, and clinicians have markedly improved patient care, continually producing cutting-edge technology and research findings. While these exciting discoveries undoubtedly bring hope for the outcomes of patients, it is also critical to look to the past to find answers. The unexpected resurgence of research into cadaveric growth hormone (c-hGH) serves as a poignant reminder of the importance of sustained vigilance in the field of medicine.

Hormone therapy has been life-changing for individuals with restricted growth caused by disorders such as growth hormone deficiency, Turner syndrome, and Noonan syndrome, among many others. Hormone therapy for growth disorders typically involves the administration of human growth hormone, a naturally occurring hormone that stimulates the development of muscle and bone. In the mid to late 1900s, cadaveric growth hormone (c-hGH) emerged as a common form of usable human growth hormone; c-hGH was collected directly from the pituitary glands of cadavers and injected into patients with a range of growth disorders over the course of a few weeks. This treatment produced consistent results for those suffering from physical underdevelopment and was used to treat over 1,500 patients in the UK. However, the use of c-hGH was abruptly halted in 1985 when researchers found that some of the c-hGH samples had been contaminated with proteins that caused Creutzfeldt-Jakob disease (CJD) during the cadaveric extraction process. CJD is a neurodegenerative condition that causes bleeding in the brain, mass neural cell damage, and ultimately death. Due to the deaths of the patients who were treated with contaminated samples, doctors turned to a synthetically created replica of human growth hormone, which would not pose similar risks.

Decades later, researchers made a startling revelation—c-hGH therapy was not only linked to CJD but also showed signs of causing early-onset Alzheimer's. Researchers observed memory loss, confusion concerning time and place, and irritability consistent with Alzheimer’s disease in c-hGH patients in their 30s, 40s, and 50s—unnaturally young ages to develop the disease. The connection between these patients and c-hGH administration suggests that Alzheimer’s disease had presumably been transmitted through the c-hGH hormone therapy, making this the first documented case of medically transmitted Alzheimer’s. The discovery was made through brain scans of some patients who were treated with c-hGH and exhibited significant amyloid plaque buildup in their neural blood vessels. Amyloid plaque, which consists of misfolded proteins that form in between neural cells, can cause brain bleeds by straining blood vessels to the point of rupture and is widely regarded as a precursor to the development of Alzheimer’s disease. 

Researchers theorize that the proteins that resulted in the amyloid plaque buildup had been unknowingly extracted from the cadavers along with c-hGH, in a manner similar to the CJD proteins. Using preserved samples of the original c-hGH injections, they identified the amyloid-beta protein. When injected into mice, this protein resulted in extensive development of amyloid plaque and subsequent brain bleeds, as hypothesized. This unintentional insight into the mechanism of Alzheimer's development revealed that Alzheimer’s may share similar functionalities with prion diseases, a group of neurological disorders (including CJD). Prion diseases occur when mutated proteins interact with normal cellular proteins and cause them to misfold and clump up, resulting in neural cell death. In the case of Alzheimer’s, these problematic proteins seem to be the recently discovered amyloid-beta proteins.

The unprecedented revelation that Alzheimer's is, on some level, akin to prion diseases offers a promising stepping stone for researchers to better understand this complex neurodegenerative condition. It is especially exciting because prion diseases are comparatively better understood than Alzheimer’s is, especially in terms of their molecular origins, providing a strong reference point for unraveling the mysteries of Alzheimer's.

Those patients who passed away from CJD or developed Alzheimer's at an early age as a result of c-hGH therapy will continue to be grave warnings of the possible negative effects of medical intervention. However, the study of their experiences also serves as a beacon of hope for current and future patients. As breakthroughs such as this one illuminate more about the ways in which Alzheimer’s functions, the potential to develop an effective treatment in the future looks more and more promising. 

The case of c-hGH therapy underscores the need for perpetual diligence and, when necessary, self-revision in the medical field. By acknowledging past mistakes and leveraging the knowledge gained, the medical community can pave the way for advancements that benefit generations to come. The persistence and intellectual curiosity of the scientific community inspire hope in solving complex medical challenges.