A disturbing case of "mad medicine": Patients treated decades ago with human growth hormone developed early-onset Alzheimer's disease, suggesting the frightening transmissibility of this devastating disorder

In a disturbing medical detective story, researchers have linked cases of early-onset Alzheimer's disease to childhood growth hormone treatments from cadaver-derived pituitary glands. The findings suggest that, like Creutzfeld-Jacob disease, Alzheimer's can be transmitted by the accidental transfer of misfolded, disease-causing proteins called prions. The study raises alarming questions about the safety of past and current medical procedures and highlights our incomplete understanding of neurodegenerative diseases.

In a startling discovery, a team of doctors in the UK have traced multiple cases of early-onset dementia to childhood treatments with human growth hormone extracted from cadavers, strongly suggesting that Alzheimer's disease is transmissible under certain circumstances.¹ The findings, published in the journal Nature Medicine, underscore how much remains unknown about the causes of common neurodegenerative disorders and raise unsettling questions about the unforeseen risks of some medical treatments.

Between 1958 and 1985, approximately 1,800 British children with growth deficiencies and short stature received injections of growth hormone extracted from the pituitary glands of human cadavers.² Tragically, some of these preparations were contaminated with misfolded proteins called prions that cause the fatal brain disorder Creutzfeld-Jakob disease (CJD), leading to 80 cases of "iatrogenic" (medically-induced) CJD in the UK.³ Previous studies had detected the characteristic amyloid plaques and misfolded amyloid-beta proteins of Alzheimer's disease in the brains of several CJD patients who had died relatively young.⁴ These observations led doctors to wonder whether some growth hormone recipients who did not develop CJD might still be at risk for Alzheimer's later in life due to the inadvertent transmission of amyloid-beta "seeds."

To investigate this chilling prospect, researchers examined the medical records of eight British adults, now aged 47-57, who had received cadaver-derived growth hormone as children and had enrolled in a monitoring program for CJD.⁵ Stunningly, they discovered that six of the eight had developed early-onset Alzheimer's or its precursor, mild cognitive impairment. The patients' symptoms emerged as early as ages 38-55 and included memory loss, visual disturbances, behavioral changes, and problems with executive function and language - a diversity of presentations reflecting different patterns of pathology in the brain.⁶

Comprehensive clinical and neuropathological assessments confirmed the diagnosis of early-onset Alzheimer's in these cases, much earlier than the typical age of onset for this disease.⁷ The brains of two deceased patients showed hallmark Alzheimer's features at postmortem: extensive deposition of amyloid plaques, tau tangles, and damage to blood vessels.⁸ None of the affected individuals carried high-risk genes for inherited early-onset Alzheimer's, strengthening the case that their illnesses arose from their childhood hormone treatments.⁹

Previous studies had found that some archived batches of cadaver-derived growth hormone were contaminated with both CJD prions and significant levels of amyloid-beta.¹⁰ When injected into animal models, the tainted hormone preparations triggered Alzheimer's-like brain changes.¹¹ Together, these lines of evidence make a compelling case that the misfolded proteins were accidentally transmitted to these patients via a medical procedure, seeding a pathological process in the brain that took years or decades to manifest as dementia. Importantly, there is no evidence that Alzheimer's is contagious through ordinary contact; this event was the result of a very unusual route of exposure.

The idea of a "transmissible" form of Alzheimer's is a new and frightening concept. Like the more classically infectious CJD prions, amyloid-beta appears capable of spreading and propagating through a kind of toxic templating, corrupting healthy proteins along the way.¹² This study suggests Alzheimer's may exist in different "strains" that cause varied manifestations of disease in the unlucky recipient.¹³ While more research is needed to fully understand the mechanisms and risks, it is clear that medical procedures must be rigorously evaluated for their potential to transfer "rogue" proteins between individuals. With an aging global population, Alzheimer's is already a looming public health emergency - we must do everything we can to prevent tragic and unnecessary cases of this devastating illness.

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References

1. Gargi Banerjee et al., "Iatrogenic Alzheimer's Disease in Recipients of Cadaveric Pituitary-Derived Growth Hormone," Nature Medicine 30 (February 2024): 394-402, https://doi.org/10.1038/s41591-023-02729-2.

2. Banerjee et al., 395.

3. Ibid.

4. Zane Jaunmuktane et al., "Evidence for Human Transmission of Amyloid-β Pathology and Cerebral Amyloid Angiopathy," Nature 525 (September 2015): 247-250, https://doi.org/10.1038/nature15369.

5. Banerjee et al., "Iatrogenic Alzheimer's Disease," 395.

6. Ibid., 396-397.

7. Ibid., 397.

8. Ibid., 399.

9. Ibid., 398.

10. Silvia A. Purro et al., "Transmission of Amyloid-β Protein Pathology from Cadaveric Pituitary Growth Hormone," Nature 564 (December 2018): 415-419, https://doi.org/10.1038/s41586-018-0790-y.

11. Purro et al.

12. Banerjee et al., "Iatrogenic Alzheimer's Disease," 400.

13. Ibid.