August 20, 2026

expert reaction to opinion piece and literature review about risk of transmission of amyloid β pathology via transfused blood products

An opinion piece and literature review published in The Lancet looks at the risk of amyloid beta transmission through transfused blood products. 

Dr Susan Kohlhaas, Executive Director of Research and Partnerships, Alzheimer’s Research UK, said:

“This research explores an interesting and important scientific question, and it’s right that researchers discuss and continue to investigate it.

“The authors bring together evidence suggesting that amyloid-beta, a protein linked to Alzheimer’s disease and cerebral amyloid angiopathy (CAA), can in very rare circumstances, be transmitted through certain, mainly historic, medical procedures.  They discuss the potential that amyloid-beta might be transmitted via blood transfusions: if it were, it is not clear how significant any risk might be.

“What this review does is identify an important gap in our knowledge.  The authors make the case for specific research to establish whether transmission through blood is occurring, who might be most at risk, and whether measures are needed to reduce that risk.  At present, we simply don’t have enough evidence to answer those questions, which is why this is important, and more research is needed.

“Importantly, this does not mean that Alzheimer’s disease is contagious.  The review does not show that receiving a blood transfusion causes Alzheimer’s disease.  Blood transfusion is a vital and often life-saving treatment, and strict measures are already in place to prevent transmission of diseases which are known to be carried in the blood, e.g. some forms of hepatitis.  People who need transfusions should continue to receive them, and to follow the advice of their medical team.”

Prof Sir John Hardy, Professor of Neuroscience and Group Leader at the UK Dementia Research Institute, UCL, said:

“There is a demonstrated risk of amyloid pathology transmission through amyloid containing tissues.  It is likely the risk through blood transfusion is small (see reference 65 from the paper) but until this is investigated systematically we don’t know what it is. We need to be clear that this potential risk is not, for example, to the caregivers of Alzheimer cases but rather through tissue donation.”

Prof Bart De Strooper FMedSci, Group Leader, UK Dementia Research Institute, UCL, said:

“There is no new material or data here – this is an opinion piece based on a review of other data.  This new opinion piece also contradicts the conclusions made in some of those previous papers^1,2,3,4 by some of the same authors, which had found there was no clear evidence of transmission of amyloid-beta through blood products.  That previous research has been taken as evidence in this opinion piece, but it had only raised a question.

“In the previous studies, the number of possible cases was very small – and the signal was only for cerebral amyloid angiopathy (CAA, a build-up of amyloid within the walls of small blood vessels near the brain surface).  That signal was small and would need to be confirmed through research – we don’t know yet that this is something that happens or that ought to be a concern or that there would need to be any mitigation against.

“We do need more research in this area, but to make any parallels with prions is in my view premature and risks unwarranted public fear without the evidence to back it up.

“It would be premature at this stage to worry about amyloid-beta transmission through blood transfusion – we don’t have convincing evidence.”

1 JAMA Preliminary Communications, ‘Intracerebral Hemorrhage Among Blood Donors and Their Transfusion Recipients’, 2023: https://jamanetwork.com/journals/jama/fullarticle/2809417

2 Lancet Neurology, ‘Potential human transmission of amyloid β pathology: surveillance and risks’, 2020: https://pubmed.ncbi.nlm.nih.gov/32949547/

3 Neural Regeneration Research, ‘Transmission of amyloid-β pathology in humans: a perspective on clinical evidence’, 2023: https://pmc.ncbi.nlm.nih.gov/articles/PMC10503612/

4 Journal of Neurology, Neurosurgery and Psychiatry, ‘Iatrogenic cerebral amyloid angiopathy: a scoping review’, 2026: https://jnnp.bmj.com/content/early/2026/08/13/jnnp-2026-339381

Dr Richard Oakley, Associate Director of Research and Innovation at Alzheimer’s Society, said:

“This opinion piece does not present any new evidence that amyloid beta, a protein linked to Alzheimer’s disease, can be transferred between people.  Instead, it highlights the importance of ensuring the quality of the blood people receive through transfusions.

“Although there is no evidence that you can ‘catch’ Alzheimer’s disease through medical procedures, ongoing research is important in ensuring they are as safe as possible.  We need to continue developing sensitive tests to clarify whether amyloid beta can be transferred.  Monitoring people who have received blood transfusions over a longer period would also help assess any risk.

“It’s important to remember that even if amyloid beta has been transferred, there is no current evidence suggesting this could lead to Alzheimer’s disease.  Blood transfusions continue to save millions of lives across the world each year.  If you need a blood transfusion, then the risk of not having one by far outweighs any risk of ‘catching’ Alzheimer’s.”

Prof Tara Spires-Jones, Division Lead in the UK Dementia Research Institute, University of Edinburgh, said:

“This paper in the Lancet is an opinion piece that does not provide new data but summarizes studies indicating a potential risk of transmitting the pathological protein amyloid beta through blood transfusions.  Amyloid beta protein forms pathological clumps called plaques in the brains of people with Alzheimer’s disease and in both Alzheimer’s and in some people with who have strokes with brain bleeding, the same protein clumps along blood vessels in pathology called cerebral amyloid angiopathy.  The core argument of the opinion piece is that it is possible that amyloid beta in blood could cause pathology in the brains of people who receive blood transfusions, but the evidence so far for this is very limited.  More work is needed to confirm whether amyloid beta in blood poses any risk for transfusion recipients and how if there is a risk, this might be mitigated.

“Authors of this opinion paper summarize studies showing that worldwide around 100 people have developed amyloid pathology on their blood vessels after treatment with either growth hormone derived from post-mortem human brain tissue or transplant of meningeal tissue (which directly touches the brain).  While this evidence that amyloid pathology from donor brain tissue can seed amyloid pathology in tissue donors is strong, these procedures are no longer used in medicine.  The authors also describe a more recent study showing that people who received blood transfusions from donors who later had multiple haemorrhagic strokes were more likely to have a stroke themselves than people who had blood transfusions from donors without stroke or a single stroke.  This hints that there could be something in the blood transfusions that increases stroke risk, but this study did not directly link the risk to amyloid beta protein or vascular amyloid pathology, and the authors of the study highlighted several important limitations of the findings including differences in follow up times between groups and that the occurrence of multiple strokes was rare.  Other studies have shown that only 20% of people who have haemorrhagic strokes also have cerebral amyloid angiopathy in their brains, with more of these strokes being caused by high blood pressure.  While it is possible that amyloid beta in the blood contributed to the results linking transfusion from people with strokes to risk of future stroke, this will need future work to confirm.”

‘Risk of transmission of amyloid β pathology via transfused blood products’ by Gargi Banerjee et al. was published in the Lancet at 23:30 UK time on Thursday 20 August 2026. 

DOI: 10.1016/S0140-6736(26)00767-1

Declared interests

Dr Susan Kohlhaas: “The only connection is that Professor Jonathan Schott, who is an author on the paper, is Chief Medical Officer at Alzheimer’s Research UK.

Just to stress, though, we had no involvement in the publication and are not connected to it.”

Prof Sir John Hardy: “No c.o.i.”

Prof Bart De Strooper: “B.D.S. is or has been, a paid consultant for Muna Therapeutics, Eli Lilly, Biogen, Janssen Pharmaceuticals, Eisai, AbbVie and other major pharmaceutical and biotechnology companies.  B.D.S is a scientific founder of Augustine Therapeutics and a scientific founder and a minor stockholder of Muna Therapeutics.  I have no conflict of interest with any statements regarding blood products.”

Prof Tara Spires-Jones: “Author of ‘Fighting for our Minds: The neuroscience of defeating dementia’.

I have no conflicts with this study but have received payments for consulting, grant reviews, scientific talks, or collaborative research over the past 10 years from AbbVie, Sanofi, Merck, Autifony, Scottish Brain Sciences, Jay Therapeutics, Cognition Therapeutics, Ono, Novo Nordisk, Eisai, Boehringer Ingelheim, and Bristol-Meyers Squibb and direct a company Spires-Jones Neuroscience, Ltd to act as a consultant.  I am also Charity trustee for the British Neuroscience Association and serve as scientific advisor to several charities and non-profit institutions.  My group receives grant funding for research from the UK Dementia Research Institute, Alzheimer’s Research UK, Alzheimer’s Society, Medical Research Council, and the Foundations for the National Institutes of Health.”

For all other experts, no reply to our request for DOIs was received.