SWAlexander
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Excerpt:
We previously reported human transmission of Aβ pathology and CAA in relatively young adults who had died of iatrogenic Creutzfeldt–Jakob disease (iCJD) after childhood treatment with cadaver-derived pituitary growth hormone (c-hGH) contaminated with both CJD prions and Aβ seeds.
Although prion diseases are transmissible conditions, the large majority of human prion disease actually occurs as a late-onset sporadic condition, sporadic Creutzfeldt–Jakob disease (CJD), and almost all other cases result from autosomal dominant coding mutations in the prion protein gene (PRNP), causing the inherited prion diseases. Acquired or iatrogenic CJD is rare, currently accounting for approximately 1% of recognized cases. Iatrogenic CJD arises from accidental inoculation with prions during medical or surgical procedures. These include former use of human cadaveric pituitary-derived growth hormone or gonadotrophin, dura mater and corneal grafting and via contaminated neurosurgical instruments.
A novel human acquired prion disease, variant CJD, arose in the 1990s, following dietary exposure to the zoonotic prion disease of cattle, bovine spongiform encephalopathy (BSE)
Between 1959 and 1985, at least 1,848 patients in the United Kingdom were treated with human cadaveric pituitary-derived growth hormone (c-hGH)13. Worldwide, over 200 cases of iatrogenic CJD have occurred as a consequence of childhood treatment with c-hGH14, with 80 cases recorded in the United Kingdom15. We first reported human-to-human transmission of Aβ pathology in people who had received c-hGH in childhood and died of iatrogenic CJD11; we later demonstrated that some of the archived batches of c-hGH used to treat these people contained measurable quantities of Aβ (and tau) and that this historical material still contained Aβ seeding activity able to transmit pathology to mice12. These experiments provided clear evidence that iatrogenic Aβ transmission had occurred in people treated with c-hGH. Multiple postmortem reports of iatrogenic Aβ transmission caused by c-hGH16,17,18 (and also via other routes16,19,20,21,22,23,24) were subsequently made by others.
https://www.nature.com/articles/s41591-023-02729-2
There is an updated version, only available by pay:
We previously reported human transmission of Aβ pathology and CAA in relatively young adults who had died of iatrogenic Creutzfeldt–Jakob disease (iCJD) after childhood treatment with cadaver-derived pituitary growth hormone (c-hGH) contaminated with both CJD prions and Aβ seeds.
Although prion diseases are transmissible conditions, the large majority of human prion disease actually occurs as a late-onset sporadic condition, sporadic Creutzfeldt–Jakob disease (CJD), and almost all other cases result from autosomal dominant coding mutations in the prion protein gene (PRNP), causing the inherited prion diseases. Acquired or iatrogenic CJD is rare, currently accounting for approximately 1% of recognized cases. Iatrogenic CJD arises from accidental inoculation with prions during medical or surgical procedures. These include former use of human cadaveric pituitary-derived growth hormone or gonadotrophin, dura mater and corneal grafting and via contaminated neurosurgical instruments.
A novel human acquired prion disease, variant CJD, arose in the 1990s, following dietary exposure to the zoonotic prion disease of cattle, bovine spongiform encephalopathy (BSE)
Between 1959 and 1985, at least 1,848 patients in the United Kingdom were treated with human cadaveric pituitary-derived growth hormone (c-hGH)13. Worldwide, over 200 cases of iatrogenic CJD have occurred as a consequence of childhood treatment with c-hGH14, with 80 cases recorded in the United Kingdom15. We first reported human-to-human transmission of Aβ pathology in people who had received c-hGH in childhood and died of iatrogenic CJD11; we later demonstrated that some of the archived batches of c-hGH used to treat these people contained measurable quantities of Aβ (and tau) and that this historical material still contained Aβ seeding activity able to transmit pathology to mice12. These experiments provided clear evidence that iatrogenic Aβ transmission had occurred in people treated with c-hGH. Multiple postmortem reports of iatrogenic Aβ transmission caused by c-hGH16,17,18 (and also via other routes16,19,20,21,22,23,24) were subsequently made by others.
https://www.nature.com/articles/s41591-023-02729-2
There is an updated version, only available by pay: