This article reports on the development of Alzheimer's disease (AD) in individuals who received cadaveric pituitary-derived growth hormone (c-hGH) contaminated with amyloid-beta (Aβ) seeds. The study highlights that AD, like Creutzfeldt-Jakob disease (CJD), can have iatrogenic (acquired through medical procedures) forms. The research team identified eight individuals who developed dementia and biomarker changes consistent with AD, suggesting that Aβ transmission via contaminated c-hGH may lead to iatrogenic AD. These patients, who had received c-hGH prepared using the HWP method, showed clinical and pathological features of AD, including amyloid-beta deposition and neurofibrillary tangles. The study emphasizes the need to review measures to prevent accidental transmission of pathogens through medical procedures. The findings suggest that Aβ assemblies may exhibit structural diversity similar to prions, and that therapeutic strategies targeting these assemblies could lead to the selection of minor components and resistance development. The study also discusses the potential role of Aβ strains in the differences between iatrogenic and sporadic Alzheimer's disease, and highlights the importance of understanding the mechanisms of prion-like diseases in neurodegenerative disorders. The research underscores the need for further investigation into the clinical and pathological features of iatrogenic Alzheimer's disease.This article reports on the development of Alzheimer's disease (AD) in individuals who received cadaveric pituitary-derived growth hormone (c-hGH) contaminated with amyloid-beta (Aβ) seeds. The study highlights that AD, like Creutzfeldt-Jakob disease (CJD), can have iatrogenic (acquired through medical procedures) forms. The research team identified eight individuals who developed dementia and biomarker changes consistent with AD, suggesting that Aβ transmission via contaminated c-hGH may lead to iatrogenic AD. These patients, who had received c-hGH prepared using the HWP method, showed clinical and pathological features of AD, including amyloid-beta deposition and neurofibrillary tangles. The study emphasizes the need to review measures to prevent accidental transmission of pathogens through medical procedures. The findings suggest that Aβ assemblies may exhibit structural diversity similar to prions, and that therapeutic strategies targeting these assemblies could lead to the selection of minor components and resistance development. The study also discusses the potential role of Aβ strains in the differences between iatrogenic and sporadic Alzheimer's disease, and highlights the importance of understanding the mechanisms of prion-like diseases in neurodegenerative disorders. The research underscores the need for further investigation into the clinical and pathological features of iatrogenic Alzheimer's disease.