A review and opinion article in The Lancet has raised the possibility that blood transfusions could, under rare and as-yet unproven circumstances, transmit amyloid-beta pathology associated with Alzheimer’s disease and cerebral amyloid angiopathy. Led by researchers from University College London and University College London Hospitals, the article does not claim that modern blood transfusions cause dementia or brain haemorrhages. Instead, it examines a combination of epidemiological observations and historical medical evidence and asks whether additional precautionary measures should be considered while scientists work to determine whether amyloid-beta can be transmitted through contemporary blood products.
Blood transfusion is one of modern medicine’s most important and frequently life-saving treatments. Millions of transfusions are administered globally each year to patients undergoing surgery, cancer treatment, trauma care and treatment for severe anaemia or blood disorders. Current blood-safety systems are designed to screen for infectious agents, prevent incompatible transfusions and reduce other known hazards. The concern discussed in the new paper is different: amyloid-beta is not a conventional virus or bacterium, but a protein that can misfold, accumulate in tissue and potentially act as a seed for further abnormal protein aggregation. Whether such material can survive blood processing and produce disease after transfusion remains uncertain.
Amyloid-beta is a small protein fragment generated when a larger membrane protein, known as amyloid precursor protein, is metabolised. In Alzheimer’s disease, amyloid-beta can accumulate in the brain as extracellular plaques, while in cerebral amyloid angiopathy, or CAA, deposits form in the walls of small and medium-sized blood vessels. These deposits weaken the vessels and can make them susceptible to microbleeds or larger intracerebral haemorrhages. The biology is complex: amyloid-beta pathology develops gradually over many years, and the presence of the protein alone does not necessarily mean that a person will develop dementia or a stroke. Genetic factors, age, vascular health and other molecular processes also influence risk.
The authors point to a large Scandinavian epidemiological study published in 2023 as one reason for examining the issue more closely. That study reported that people who received blood from donors who later developed multiple brain haemorrhages appeared to have a higher risk of experiencing brain haemorrhages themselves. Multiple haemorrhages can be a clinical marker of CAA, although they can also arise through other mechanisms. The study was observational, meaning that it identified an association rather than demonstrating that transfusion caused the later disease. Differences between donors and recipients, shared risk factors, medical histories and statistical limitations could all contribute to the result. Nevertheless, the finding has prompted questions about whether a transmissible biological factor might be involved.
The possibility is also informed by rare cases in which amyloid-beta pathology was unintentionally transferred during historical medical procedures. Iatrogenic CAA was first recognised in living patients who had received transplants of cadaveric dura mater during childhood. Dura mater is the tough membrane surrounding the brain and spinal cord. Decades after those procedures, some individuals developed CAA and brain haemorrhages at unusually young ages. Similar cases have since been reported internationally. The original tissue preparations were produced before researchers understood that abnormal proteins could persist in biological materials and potentially initiate pathology in a recipient.
Further evidence emerged from patients treated during childhood with cadaveric pituitary-derived human growth hormone, or c-hGH. Before recombinant growth hormone became available, some countries used hormone extracted from the pituitary glands of deceased individuals. In 2024, Professor John Collinge and colleagues reported five patients who developed symptoms consistent with early-onset Alzheimer’s disease decades after receiving c-hGH. A subsequent report described another patient whose diagnosis was confirmed at autopsy, including characteristic Alzheimer’s pathology. These cases suggest that amyloid-beta seeds may have been present in contaminated hormone preparations alongside the prion protein responsible for Creutzfeldt-Jakob disease. The treatment was discontinued in the United Kingdom in 1985, while cadaveric dura mater grafts were stopped in 1992.
Such historical cases demonstrate that amyloid-beta pathology can be transferred in exceptional circumstances, but they do not establish that ordinary transfusions transmit Alzheimer’s disease. The exposure routes, doses, tissue conditions and processing methods involved in the older treatments were unlike those used for modern blood components. In addition, the incubation period may extend for several decades, making the effects difficult to detect through routine surveillance. Researchers still face major technical challenges in measuring amyloid-beta infectivity. Standard tests can identify amyloid deposits or related biomarkers, but detecting very small quantities of biologically active seeding material in blood is considerably more difficult. A positive molecular signal would not automatically demonstrate that the material could cause disease.
The Lancet article places the debate in the context of the United Kingdom’s Infected Blood Inquiry, which examined how thousands of people were infected with HIV and hepatitis C through contaminated blood and blood products. The inquiry concluded that much of the resulting harm was avoidable and highlighted the consequences of delayed action when potential risks are not fully understood. It also discussed the response to variant Creutzfeldt-Jakob disease, a rare neurological disorder caused by misfolded prion proteins. The United Kingdom introduced measures including leukodepletion, a process that removes most white blood cells from donated blood, when the threat was still largely theoretical. White blood cells were considered a possible carrier of the infectious prion agent, although leukodepletion was not designed specifically to remove amyloid-beta.
The authors argue that this history supports a precautionary approach, including transparent communication, improved surveillance and research into whether amyloid-beta seeds are present in blood and remain biologically active after processing. Possible safety measures would need to be evaluated carefully because every intervention in the blood supply can have costs, logistical effects and unintended consequences. At present, there is no evidence that patients should avoid medically necessary transfusions, and the article does not recommend abandoning transfusion medicine. Instead, it calls for a systematic assessment of the potential risk before definitive conclusions are drawn. Professor Collinge said that transfusions save many lives but that all plausible hazards should be investigated thoroughly so that blood products can be made as safe as possible.
The central scientific question is therefore not whether Alzheimer’s disease is contagious in everyday life, but whether specific protein assemblies could occasionally be transferred through medical materials and later seed pathology in susceptible people. Establishing an answer will require long-term epidemiological studies, validated laboratory assays, analysis of stored blood samples and careful comparison of transfusion histories with neurological outcomes. Until those studies are completed, the evidence remains suggestive rather than conclusive. The new article seeks to ensure that uncertainty does not prevent research, while also avoiding alarm over a treatment that remains essential to modern healthcare.
Subject of Research: Potential transmission of amyloid-beta pathology through transfused blood products
Article Title: Risk of transmission of amyloid β pathology via transfused blood products
News Publication Date: 20-Aug-2026
Web References: https://doi.org/10.1016/S0140-6736(26)00767-1
References: Evidence that brain bleeds might be transmissible by blood transfusion (2023)
Keywords: Blood transfusion, amyloid-beta, Alzheimer’s disease, cerebral amyloid angiopathy, brain haemorrhage, iatrogenic disease, blood safety, prion biology, medical research, The Lancet
Tags: Alzheimer’s disease transmission risk through blood transfusionsamyloid-beta protein in bloodblood product safety and amyloid-betacerebral amyloid angiopathy and blood transfusion safetyepidemiological evidence of amyloid-beta in blood donorshistorical medical evidence of protein transmissionimpact of blood transfusions on Alzheimer’s diseasemisfolded protein seeding in neurodegenerationpotential transmission of proteinopathies via transfusionprecautionary measures for blood screeningscreening for neurodegenerative disease proteins
