{"id":293,"date":"2026-03-01T12:57:49","date_gmt":"2026-03-01T12:57:49","guid":{"rendered":"https:\/\/forgetnow.com\/index.php\/2026\/03\/01\/decades-old-medical-treatment-linked-to-five-cases-of-transmitted-alzheimers-disease-new-study-reveals\/"},"modified":"2026-03-01T12:57:49","modified_gmt":"2026-03-01T12:57:49","slug":"decades-old-medical-treatment-linked-to-five-cases-of-transmitted-alzheimers-disease-new-study-reveals","status":"publish","type":"post","link":"https:\/\/forgetnow.com\/index.php\/2026\/03\/01\/decades-old-medical-treatment-linked-to-five-cases-of-transmitted-alzheimers-disease-new-study-reveals\/","title":{"rendered":"Decades-Old Medical Treatment Linked to Five Cases of Transmitted Alzheimer\u2019s Disease, New Study Reveals"},"content":{"rendered":"

Groundbreaking research published today in the prestigious journal Nature Medicine<\/em> has brought to light an unprecedented connection between a medical treatment administered decades ago and the subsequent development of Alzheimer\u2019s disease in five individuals. The study, spearheaded by researchers at University College London (UCL) and UCL Hospitals (UCLH), identifies these cases as believed to have arisen from treatment with cadaver-derived human growth hormone (c-hGH), a practice banned globally since the 1980s due to its association with Creutzfeldt-Jakob Disease (CJD). This revelation marks a significant, albeit extremely rare, instance of potentially "iatrogenic" or medically transmitted Alzheimer’s, offering profound insights into the disease’s mechanisms.<\/p>\n

The Unveiling of an Unexpected Link<\/h3>\n

The core of the new findings centers on five individuals who, as children, received c-hGH extracted from the pituitary glands of deceased donors. This specific form of growth hormone therapy was prevalent between the 1950s and mid-1980s for treating growth hormone deficiency. The UCL and UCLH team\u2019s investigation revealed that the growth hormone batches used in these treatments had the potential to contain fragments of amyloid-beta protein, a hallmark protein intricately linked to the pathology of Alzheimer\u2019s disease. Decades after receiving these treatments, the five individuals developed symptoms consistent with Alzheimer’s disease, which were subsequently confirmed through rigorous diagnostic tests.<\/p>\n

Crucially, the research team meticulously ruled out other potential causes for these early-onset symptoms. This included genetic predispositions commonly associated with young-onset Alzheimer’s and any inherent link between growth hormone deficiency itself and the development of the neurodegenerative condition. The careful exclusion of these factors strengthens the hypothesis of a direct, iatrogenic transmission route.<\/p>\n

A Historical Context: The c-hGH Saga and the CJD Precedent<\/h3>\n

To fully grasp the gravity of this discovery, it is essential to understand the historical context surrounding c-hGH. From the mid-20th century, c-hGH was a crucial treatment for children suffering from severe growth hormone deficiency, a condition that could lead to dwarfism if left untreated. The hormone, extracted from the pituitary glands of thousands of cadavers, was seen as a medical marvel, offering hope and normal development to affected children.<\/p>\n

However, the safety of c-hGH came under intense scrutiny in the mid-1980s. Concerns began to mount when recipients of the treatment started developing Creutzfeldt-Jakob Disease (CJD), a rare and fatal neurodegenerative condition caused by infectious proteins known as prions. The first confirmed case of iatrogenic CJD linked to c-hGH was reported in 1985. This discovery sent shockwaves through the medical community, leading to the immediate cessation of c-hGH use worldwide and its replacement with synthetically produced recombinant human growth hormone (rhGH), which carries no such transmission risks. In the UK alone, approximately 1,800 people received c-hGH treatment between 1959 and 1985. Globally, estimates suggest tens of thousands received the treatment, with hundreds subsequently developing CJD. The tragic CJD cases served as a stark lesson in the potential unforeseen risks associated with biological products derived from human tissues.<\/p>\n

The current study builds upon previous research that had already hinted at a potential link between c-hGH and amyloid pathology. For instance, post-mortem examinations of individuals who died from c-hGH-transmitted CJD had shown evidence of amyloid-beta plaques in their brains, even though they had not clinically presented with Alzheimer’s symptoms. This earlier work provided a critical foundation for the present investigation, suggesting that the contaminated c-hGH might have contained amyloid seeds alongside the CJD prions.<\/p>\n

The Mechanism of Transmission: Amyloid Seeding<\/h3>\n

The concept underpinning the potential transmission of Alzheimer’s in these cases is known as "amyloid seeding." Similar to how prions propagate in CJD by inducing normal proteins to misfold, the theory suggests that minute quantities of misfolded amyloid-beta proteins, if present in the c-hGH, could have acted as "seeds." Once introduced into the brain, these seeds could then trigger the aggregation and misfolding of naturally occurring amyloid-beta proteins, initiating the cascade that leads to the formation of amyloid plaques \u2013 a hallmark pathology of Alzheimer’s disease. Over decades, this process would slowly progress, eventually leading to the widespread brain damage and cognitive decline characteristic of the disease.<\/p>\n

Dr. Gargi Banerjee, an Alzheimer\u2019s Research UK Clinical Research Fellow and part of the study\u2019s research team, underscored the specific nature of this transmission: \u201cThis transmission occurred following treatment with a now obsolete form of growth hormone, and involved repeated treatments with contaminated material, often over several years.\u201d This highlights that the exposure was significant and prolonged, increasing the likelihood of amyloid seeding.<\/p>\n

Expert Reassurance and Broader Implications<\/h3>\n

While the findings are profound, medical experts are quick to provide crucial reassurance to the public. Study co-lead Prof. Jonathan Schott, Alzheimer\u2019s Research UK\u2019s Chief Medical Officer, based at University College London, emphasized the extreme rarity of such occurrences. \u201cIt\u2019s important to stress that the circumstances through which we believe these individuals tragically developed Alzheimer\u2019s are highly unusual,\u201d he stated. He firmly reinforced that there is \u201cno risk\u201d that Alzheimer\u2019s disease can be spread between individuals through casual contact, routine medical care, or modern surgical procedures. The transmission mechanism identified is specific to the now-discontinued c-hGH treatment and its unique biological contaminants. Modern growth hormone treatments are synthetic and carry no such risk.<\/p>\n

The primary implication of this research is not one of public health alarm regarding current medical practices, but rather a significant leap in our understanding of Alzheimer’s disease itself. Dr. Susan Kohlhaas, Alzheimer\u2019s Research UK\u2019s Executive Director of Research and Partnerships, articulated this point clearly. \u201cA diagnosis of Alzheimer\u2019s disease can be devastating for all involved, and our hearts go out to the families that have been affected by these tragic circumstances,\u201d she said. \u201cDespite the small size and rare circumstances of this study, it has provided valuable insights on how amyloid can spread within the brain, providing further clues on how Alzheimer\u2019s disease progresses and potential new targets for the treatments of tomorrow.\u201d<\/p>\n

This study strengthens the amyloid hypothesis, which posits that the accumulation of amyloid-beta plaques is a central event in the pathogenesis of Alzheimer’s. Understanding that amyloid pathology can be initiated by external seeds, even in rare circumstances, provides further validation for therapeutic strategies aimed at preventing or clearing amyloid aggregation. It opens new avenues for research into the earliest stages of amyloid accumulation and how it might be interrupted.<\/p>\n

Ethical Considerations and Medical Evolution<\/h3>\n

The history of c-hGH use and its associated risks serves as a powerful reminder of the delicate balance between medical innovation and patient safety. The initial use of c-hGH was a necessity born from limited alternatives, reflecting the medical knowledge and technological capabilities of the time. The subsequent discovery of CJD transmission led to a rapid and decisive shift in medical practice, underscoring the dynamic nature of medical ethics and public health vigilance.<\/p>\n

This latest discovery prompts further reflection on the long-term consequences of medical interventions, especially those involving biological materials. It highlights the importance of robust surveillance systems and long-term follow-up studies, even decades after a treatment has been discontinued. The ability of scientific research to uncover such links, even many years later, demonstrates the enduring commitment to understanding disease and improving patient care.<\/p>\n

Public Health Outreach and Future Research<\/h3>\n

Given the historical context, public health bodies and medical organizations are keen to ensure that individuals who received c-hGH treatment are aware of these findings and have access to appropriate support and information. In the UK, individuals who were treated with c-hGH between 1959 and 1985 are encouraged to contact the National Prion Clinic. This outreach is crucial for providing guidance, addressing concerns, and potentially identifying further cases that could contribute to scientific understanding. The contact details provided are uclh.prion.help@nhs.net or by telephone at 020 7679 5142 or 020 7679 5036.<\/p>\n

Looking ahead, this study is likely to stimulate further research in several areas:<\/p>\n

    \n
  • Detailed Pathological Analysis:<\/strong> Deeper investigation into the brain tissue of these individuals could reveal more about the specific amyloid strains involved and their propagation patterns.<\/li>\n
  • Biomarker Development:<\/strong> The insights gained could aid in developing more sensitive biomarkers for early detection of amyloid pathology, particularly in individuals with unusual risk factors or early-onset symptoms.<\/li>\n
  • Therapeutic Targets:<\/strong> A better understanding of how amyloid seeds can initiate disease could lead to novel therapeutic strategies aimed at preventing the initial seeding or disrupting the subsequent aggregation process.<\/li>\n
  • Epidemiological Studies:<\/strong> While the current cases are rare, further epidemiological studies might be warranted to identify any other potential, albeit exceedingly rare, iatrogenic pathways for neurodegenerative diseases.<\/li>\n<\/ul>\n

    The discovery of iatrogenic Alzheimer\u2019s disease, though tragic for the affected individuals and their families, represents a pivotal moment in neurodegenerative research. It provides compelling evidence for the amyloid seeding hypothesis, offering a unique window into the initiation and progression of Alzheimer\u2019s disease, and ultimately, guiding the quest for more effective treatments and preventative strategies for this devastating condition.<\/p>\n","protected":false},"excerpt":{"rendered":"

    Groundbreaking research published today in the prestigious journal Nature Medicine has brought to light an unprecedented connection between a medical treatment administered decades ago and the subsequent development of Alzheimer\u2019s…<\/p>\n","protected":false},"author":1,"featured_media":292,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[2],"tags":[4,6,3,7,5],"class_list":["post-293","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-alzheimers-dementia-research","tag-alzheimers","tag-brain-health","tag-dementia","tag-geriatric-medicine","tag-memory-loss"],"_links":{"self":[{"href":"https:\/\/forgetnow.com\/index.php\/wp-json\/wp\/v2\/posts\/293","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/forgetnow.com\/index.php\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/forgetnow.com\/index.php\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/forgetnow.com\/index.php\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/forgetnow.com\/index.php\/wp-json\/wp\/v2\/comments?post=293"}],"version-history":[{"count":0,"href":"https:\/\/forgetnow.com\/index.php\/wp-json\/wp\/v2\/posts\/293\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/forgetnow.com\/index.php\/wp-json\/wp\/v2\/media\/292"}],"wp:attachment":[{"href":"https:\/\/forgetnow.com\/index.php\/wp-json\/wp\/v2\/media?parent=293"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/forgetnow.com\/index.php\/wp-json\/wp\/v2\/categories?post=293"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/forgetnow.com\/index.php\/wp-json\/wp\/v2\/tags?post=293"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}