Cadaveric pituitary-derived growth hormone delivery influences iatrogenic Alzheimer’s Disease

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recent Nature’s medicine Studies have shown that cadaver-derived pituitary growth hormone (c-hGH) receptors alter biomarkers in Alzheimer’s disease (AD). This study indicates a link between c-hGH and AD.

Study: Iatrogenic Alzheimer's disease in cadaveric pituitary-derived growth hormone recipients.  Image credit: Gorodenkoff/Shutterstock.comStudy: Iatrogenic Alzheimer’s disease in cadaveric pituitary-derived growth hormone recipients. Image credit: Gorodenkoff/


Prions are pathogenic agents that cause abnormal folding of the prion protein (PrPC), which is abundant in the brain. In mammals, prions cause neurodegenerative diseases.

Different strains of prions have been characterized to exhibit variation in fibril formation. Each structural change is responsible for specific clinicopathological disease phenotypes.

Creutzfeldt-Jakob disease (CJD) is a sporadic condition caused by infectious prions. Apart from CJD, all other prion diseases are caused by mutations in the autosomal prion protein gene (PRNP)

The prevalence of acquired or iatrogenic CJD is rare; It can occur due to accidental inoculation during a surgical procedure. About 200 cases of iatrogenic CJD have been recorded worldwide as a result of c-hGH treatment during childhood.

Previous studies have shown that the use of contaminated gonadotrophin, human cadaveric pituitary-derived growth hormone, and corneal grafting using contaminated neurosurgical instruments can lead to the development of CJD.

In the 1990s, the emergence of a novel CJD variant was documented, caused by dietary exposure to bovine spongiform encephalopathy (BSE).

Human neurodegenerative diseases, such as Parkinson’s and Alzheimer’s diseases, involve the accumulation of misfolded host proteins in a ‘prion-like’ fashion.

Previous studies have shown that the transmission of amyloid-beta (Aβ) pathology occurs via an iatrogenic route. A prolonged incubation has been associated with the development of iatrogenic cerebral amyloid angiopathy (CAA), indicating the risk of developing iatrogenic Alzheimer’s disease after a long time delay.

Previous studies have demonstrated that iatrogenic Aβ infection occurs in patients receiving c-hGH treatment. There is no clinical documentation showing that iatrogenic disease occurs due to Aβ infection in c-hGH recipients.

About the study

Brain biopsy and postmortem brain tissue samples were collected following standard neurosurgical protocols. The study cohort included individuals with all forms of prion disease, such as sporadic, inherited, iatrogenic, or variant forms.

It also included people who were at risk of developing CJD and who were treated with c-hGH. Next-generation sequencing (NGS) was performed on all test samples to assess the genetic aspect of CJD expression, especially in those who received c-hGH treatment.

Study results

Most studies have shown that AD is primarily a sporadic condition that occurs in late adult life. However, some studies have indicated its genetic nature by showing that APP, PSEN1, and PSEN2 gene mutations are associated with AD manifestations.

Taken together, the results suggest that AD is associated with a triad of etiologies, namely, sporadic, inherited and rare acquired forms, which are related to common prion diseases.

Participants who developed symptoms were repeatedly exposed to contaminated c-HGH over many years. However, the treatment was discontinued many years ago.

The transmissible nature of AD disease has been documented under certain circumstances. Experimental findings indicate that iatrogenic forms of Alzheimer’s disease are phenotypically distinct from sporadic and inherited forms.

Previous studies have demonstrated the relationship between the transmission of Aβ pathology and the manifestation of iatrogenic cerebral amyloid angiopathy (CAA).

Participants with a history of iatrogenic CAA died of iatrogenic CJD and these patients were exposed to c-hGH contaminated with Aβ seeds/tau and CJD prions.

Compared to CJD manifestations, many more people have been found to develop AD. Based on this observation, it can be hypothesized that Aβ seeds frequently contaminate c-hGH lots, which are generated from a larger pool of cadaveric pituitary glands than CJD prions.

Furthermore, individuals who were exposed to c-hGH and did not develop CJD had a higher risk of progression to develop all pathological features of AD with a longer incubation period than those who developed iatrogenic CAA.


Current studies have shown that AD has a triad of etiologies, ie, iatrogenic (environmentally acquired), late-onset sporadic, and early-onset hereditary.

The results imply the potential of targeting disease-associated assemblies as a therapeutic approach.

Although iatrogenic AD is a rare event, future studies must focus on developing measures to prevent accidental transmission of pathogenic prions during surgery with contaminated instruments.

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