A new Lancet analysis brings together human transfusion records, rare cases of medically acquired amyloid pathology, and animal experiments to examine whether amyloid beta could spread through donated blood.
The evidence raises a legitimate blood-safety question, but it does not show that modern transfusions cause Alzheimer’s disease. Researchers say better testing and long-term surveillance are needed to determine whether any measurable risk exists.
A 2026 analysis published in The Lancet has raised an important but unresolved blood safety question: could blood transfusions transmit forms of amyloid beta capable of initiating disease-related changes in the brain?
The evidence does not show that blood transfusions cause Alzheimer’s disease. Instead, researchers argue that findings from rare historical medical exposures, observational studies, and animal experiments make amyloid beta transmission through blood biologically plausible enough to investigate further (Banerjee et al., 2026).
For patients, the distinction is important. Alzheimer’s disease is not contagious, and current evidence provides no basis for avoiding a medically necessary blood transfusion because of a proposed amyloid risk.
Key Takeaways
- The 2026 Lancet publication is a peer-reviewed Viewpoint that evaluates existing evidence. It is not a new transfusion trial or patient study (Banerjee et al., 2026).
- Amyloid beta pathology has previously been associated with rare medical transmission involving cadaver-derived human material, but these historical exposures differ substantially from modern blood transfusion (Banerjee et al., 2024; Purro et al., 2018).
- A large 2023 JAMA study found a higher risk of spontaneous intracerebral hemorrhage among recipients of red blood cells from donors who later developed multiple spontaneous brain hemorrhages (Zhao et al., 2023).
- That study did not test donated blood for amyloid beta or directly diagnose cerebral amyloid angiopathy in the relevant donors and recipients (Zhao et al., 2023).
- Animal experiments support the possibility that blood can carry factors capable of accelerating amyloid pathology, but they cannot establish the risk from human transfusions (Morales et al., 2020).
- No study has demonstrated that modern blood transfusion causes Alzheimer’s dementia.
What the Lancet Analysis Actually Says
The Lancet paper examines whether amyloid beta assemblies with the ability to seed further protein aggregation could potentially be transmitted through donated blood or blood products (Banerjee et al., 2026).
The publication is a Viewpoint. Its authors did not recruit transfusion recipients, analyze a new cohort, or identify amyloid beta seeds in donated human blood and demonstrate that they subsequently caused disease.
Instead, they brought together several lines of evidence that they argue justify further investigation (Banerjee et al., 2026).
Amyloid beta is a protein fragment that can aggregate in the brain. In Alzheimer’s disease, it commonly forms plaques within brain tissue. It can also accumulate in cerebral blood-vessel walls, producing cerebral amyloid angiopathy, or CAA.
CAA can weaken blood vessels and increase the risk of intracerebral hemorrhage. Although CAA and Alzheimer’s disease frequently coexist, they are not the same condition.
That distinction matters because the strongest human evidence involving transfusion concerns brain hemorrhage and possible CAA, not transfusion-acquired Alzheimer’s dementia.
A Lancet analysis examines evidence from human records, historical medical exposures, and animal studies. Amyloid beta transmission through modern blood transfusions remains unproven.
The Strongest Human Evidence Comes From a Large Transfusion Study
In 2023, researchers published an exploratory retrospective cohort study in JAMA using nationwide blood-bank and health-register data from Sweden and Denmark (Zhao et al., 2023).
The analysis included 759,858 transfusion recipients in Sweden and 329,512 in Denmark.
Researchers investigated whether recipients of red blood cells from donors who subsequently experienced spontaneous intracerebral hemorrhage were themselves more likely to develop spontaneous intracerebral hemorrhage.
Recipients exposed to blood from donors who later experienced multiple spontaneous intracerebral hemorrhages showed a higher risk.
In Sweden, the adjusted hazard ratio was 2.73 (95% CI, 1.72 to 4.35). In Denmark, it was 2.32 (95% CI, 1.04 to 5.19) (Zhao et al., 2023).
The Swedish analysis corresponded to an estimated 30-year cumulative incidence difference of 2.3 percentage points.
The investigators did not observe a significant increase among recipients whose donors later experienced only one spontaneous hemorrhage. They also did not find the same association for ischemic stroke, which was examined as a negative-control outcome (Zhao et al., 2023).
Why the Study Does Not Prove Amyloid Transmission
Despite the size of the databases, the number of relevant events among exposed recipients was small. There were 18 primary outcome events in the principal Swedish multiple-hemorrhage donor group and six in the corresponding Danish group (Zhao et al., 2023).
Investigators also did not test the transfused blood for amyloid beta seeds or directly establish CAA in the relevant donors and recipients.
Repeated spontaneous intracerebral hemorrhage was used as an indirect marker for possible CAA because vascular amyloid can cause recurrent brain bleeding.
The association could be compatible with transmission of an amyloid-related factor, but it does not establish that explanation. Residual confounding, selection effects, or another unidentified biological factor could also contribute (Zhao et al., 2023).
What Historical Medical Exposures Tell Us
Stronger evidence that amyloid beta pathology can be medically acquired comes from unusual treatments used decades ago.
Before synthetic growth hormone became available, some children received human growth hormone extracted from pituitary glands collected from deceased donors. Certain preparations were contaminated with prions and caused iatrogenic Creutzfeldt-Jakob disease.
Researchers later found substantial amyloid beta deposition and CAA in some recipients.
Archived samples of cadaver-derived growth hormone were subsequently found to contain amyloid beta. When material from these preparations was inoculated directly into the brains of susceptible mice, it seeded amyloid beta pathology (Purro et al., 2018).
In 2024, researchers reported dementia in several former recipients of cadaver-derived growth hormone and interpreted the findings as evidence of a rare, medically acquired form of Alzheimer’s disease (Banerjee et al., 2024).
That interpretation has been challenged. Nath and colleagues argued that the available amyloid and tau evidence was insufficient to establish Alzheimer’s disease in all of the reported cases (Nath et al., 2024).
The disagreement reinforces an important distinction. Evidence for medically acquired amyloid beta pathology does not necessarily establish transmission of the complete clinical and pathological syndrome of Alzheimer’s disease.
These historical exposures also differ substantially from modern transfusion. Cadaver-derived growth hormone involved pooled biological material obtained from human pituitary glands. Blood transfusion involves different tissues, processing methods, storage conditions, concentrations, and routes of exposure.
Two CAA Cases Raised Another Transfusion Question
In 2024, researchers reported two people who had received red blood cell transfusions during infancy and later developed CAA at ages 47 and 57 (Kaushik et al., 2024).
Their relatively young ages and long intervals between transfusion and disease made the histories noteworthy.
However, two cases cannot establish causation. There were no implicated donors, stored blood units, or molecular evidence connecting donor material with the patients’ vascular amyloid. Blood transfusions are also common, while CAA can develop without an identifiable medical source.
The cases add to the rationale for studying transfusion as a possible source of iatrogenic CAA, but they do not demonstrate that transfusions caused either patient’s disease (Kaushik et al., 2024).
What Animal Experiments Show
Morales and colleagues studied blood from older transgenic mice with substantial cerebral amyloidosis. Whole blood or plasma was infused into younger transgenic mice susceptible to amyloid pathology (Morales et al., 2020).
The exposed animals subsequently showed accelerated brain amyloidosis and increased neuroinflammation.
The experiment supports the possibility that blood can carry material capable of influencing amyloid pathology. It does not establish that the effect was caused exclusively by circulating amyloid beta seeds, nor does it reproduce routine human transfusion (Morales et al., 2020).
Genetically engineered mice can also be considerably more susceptible to amyloid deposition than typical human recipients.
Animal evidence therefore establishes biological plausibility under experimental conditions. It does not establish the magnitude, or even the existence, of a corresponding risk from modern human transfusion.
Why Prion History Matters but Is Not Proof
There is a precedent for blood transmission of an abnormal protein associated with neurodegenerative disease.
UK surveillance identified cases of variant Creutzfeldt-Jakob disease, or vCJD, following transfusion from donors who subsequently developed vCJD. Urwin et al. (2016) reported three clinical vCJD cases among 67 identified recipients of blood components from such donors, as well as another recipient with abnormal prion protein detected postmortem.
This history demonstrates why rare diseases with long incubation periods can be difficult to identify through conventional blood-safety surveillance.
However, prions and amyloid beta should not be treated as equivalent.
Prions are established infectious agents capable of transmitting prion disease. Amyloid beta has demonstrated self-propagating or “prion-like” properties experimentally, but routine transmission between people has not been established.
Nothing in this research suggests that Alzheimer’s disease spreads through touching, caregiving, coughing, sexual contact, sharing food, or living with someone who has dementia.
What Researchers Still Need to Establish
A convincing case for transfusion-associated amyloid disease would require several pieces of evidence to converge.
Researchers would need to show that biologically active amyloid beta seeds are present in donor blood, survive collection and processing, remain active after transfusion, and can ultimately initiate relevant pathology in human recipients.
Epidemiological findings would also need independent replication, ideally alongside amyloid biomarkers, brain imaging, neuropathology, and stored donor or recipient samples.
Researchers would then have to determine whether any such exposure actually produces clinically meaningful disease rather than silent pathology.
At present, that causal chain has not been demonstrated (Banerjee et al., 2026).
What This Means for Patients and Blood Safety
Blood transfusions are used for severe blood loss, anemia, cancer-related complications, surgery, trauma, obstetric hemorrhage, and other potentially life-threatening conditions.
Their clinical benefits are established. In contrast, the proposed risk from amyloid beta transmission remains unconfirmed and cannot currently be quantified.
Current evidence does not establish amyloid beta transmission as a recognized risk of modern blood transfusion and does not provide a scientific basis for avoiding a medically necessary transfusion because of this hypothesis.
For blood services, the findings justify continued research and surveillance.
There is currently no validated donor-screening test that determines whether a blood component contains seeding-competent amyloid beta capable of transmitting pathology. Conventional Alzheimer’s blood biomarkers should not be assumed to measure transmissibility (Banerjee et al., 2026).
Frequently Asked Questions
Can Alzheimer’s disease be transmitted through a blood transfusion?
No study has demonstrated that modern blood transfusions transmit Alzheimer’s disease. Researchers are investigating whether biologically active amyloid beta could potentially be transmitted through blood and contribute to amyloid pathology, particularly CAA. This remains an unproven hypothesis (Banerjee et al., 2026).
What did the blood-transfusion study actually find?
A 2023 study found that recipients of red blood cells from donors who later experienced multiple spontaneous intracerebral hemorrhages had a higher risk of spontaneous intracerebral hemorrhage themselves (Zhao et al., 2023). The researchers did not detect amyloid beta in the donated blood or prove that amyloid transmission caused the association.
Has amyloid beta ever been transmitted between people?
Evidence indicates that amyloid beta pathology can be acquired through exceptional historical medical exposures involving cadaver-derived human material (Banerjee et al., 2024; Purro et al., 2018). These exposures were very different from modern blood transfusion and do not suggest that Alzheimer’s disease spreads through ordinary human contact.
Is Alzheimer’s disease contagious?
No. There is no evidence that Alzheimer’s disease spreads through touching, caregiving, coughing, sexual contact, sharing food, or living with someone who has dementia. The transmission question concerns unusual medical exposure to potentially seeding-competent biological material, not ordinary person-to-person contact (Banerjee et al., 2026).
Should people avoid blood transfusions because of this research?
Current evidence does not establish amyloid beta transmission as a recognized risk of modern blood transfusion. The research therefore does not provide a scientific basis for avoiding a medically necessary transfusion because of this proposed risk. Patients concerned about a planned transfusion should discuss its established benefits, risks, and appropriate alternatives with their healthcare team.
Final Thoughts
The possibility that amyloid beta pathology could be transmitted through blood deserves careful investigation, but the evidence has not established that this occurs with modern transfusions.
Historical medical exposures show that amyloid beta pathology can be acquired under exceptional circumstances. Animal experiments provide biological plausibility, while the large Scandinavian transfusion study identified an association that warrants further investigation.
None completes the causal chain from donated human blood to amyloid disease in a recipient.
For now, the evidence supports continued research and blood-safety surveillance, not the conclusion that blood transfusions transmit Alzheimer’s disease.
References
Banerjee, G., Edgren, G., Zhao, J., Ferguson, N. M., Harvala, H., Hope, J., Jackson, G. S., Lowry, P. J., Mead, S., Purro, S. A., Schott, J. M., Turner, M. L., Werring, D. J., Zetterberg, H., & Collinge, J. (2026). Risk of transmission of amyloid β pathology via transfused blood products. The Lancet, 408(10556), 753–760. https://doi.org/10.1016/S0140-6736(26)00767-1
Banerjee, G., Farmer, S. F., Hyare, H., Jaunmuktane, Z., Mead, S., Ryan, N. S., Schott, J. M., Werring, D. J., Rudge, P., & Collinge, J. (2024). Iatrogenic Alzheimer’s disease in recipients of cadaveric pituitary-derived growth hormone. Nature Medicine, 30(2), 394–402. https://doi.org/10.1038/s41591-023-02729-2
Kaushik, K., Wermer, M. J. H., & van Etten, E. S. (2024). Cerebral amyloid angiopathy decades after red blood cell transfusions: A report of two cases from a prospective cohort. European Journal of Neurology, 31(6), Article e16277. https://doi.org/10.1111/ene.16277
Morales, R., Duran-Aniotz, C., Bravo-Alegria, J., Estrada, L. D., Shahnawaz, M., Hu, P. P., Kramm, C., Morales-Scheihing, D., Urayama, A., & Soto, C. (2020). Infusion of blood from mice displaying cerebral amyloidosis accelerates amyloid pathology in animal models of Alzheimer’s disease. Acta Neuropathologica Communications, 8(1), Article 213. https://doi.org/10.1186/s40478-020-01087-1
Nath, A., Holtzman, D. M., Miller, B. L., Grinberg, L. T., & Leschek, E. W. (2024). Insufficient evidence for an association between iatrogenic Alzheimer’s disease and cadaveric pituitary-derived growth hormone. Alzheimer’s & Dementia, 20(10), 7399–7402. https://doi.org/10.1002/alz.14127
Purro, S. A., Farrow, M. A., Linehan, J., Nazari, T., Thomas, D. X., Chen, Z., Mengel, D., Saito, T., Saido, T., Rudge, P., Brandner, S., Walsh, D. M., & Collinge, J. (2018). Transmission of amyloid-β protein pathology from cadaveric pituitary growth hormone. Nature, 564(7736), 415–419. https://doi.org/10.1038/s41586-018-0790-y
Urwin, P. J., Mackenzie, J. M., Llewelyn, C. A., Will, R. G., & Hewitt, P. E. (2016). Creutzfeldt-Jakob disease and blood transfusion: Updated results of the UK Transfusion Medicine Epidemiology Review Study. Vox Sanguinis, 110(4), 310–316. https://doi.org/10.1111/vox.12371
Zhao, J., Rostgaard, K., Lauwers, E., Dahlén, T., Ostrowski, S. R., Erikstrup, C., Pedersen, O. B., De Strooper, B., Lemmens, R., Hjalgrim, H., & Edgren, G. (2023). Intracerebral hemorrhage among blood donors and their transfusion recipients. JAMA, 330(10), 941–950. https://doi.org/10.1001/jama.2023.14445
Disclosure
The author declares no financial, professional, or personal conflicts of interest related to this article. No external organization funded or influenced its preparation.
