Gargi Banerjee, Gustaf Edgren, Jingcheng Zhao, Neil M Ferguson, Heli Harvala, James Hope, Graham S Jackson, Philip J Lowry, Simon Mead, Silvia A Purro, Jonathan M Schott, Marc L Turner, David J Werring, Henrik Zetterberg, John Collinge
Seeded protein misfolding and aggregation are relevant to many neurodegenerative diseases. The archetype are prions: protein-only infectious agents that cause fatal neurodegenerative diseases including Creutzfeldt-Jakob disease (CJD). The recent recognition of iatrogenic amyloid β cerebral amyloid angiopathy (CAA) and Alzheimer's disease, caused by inadvertent seeding of amyloid β pathology following historical medical procedures, raises concerns that these conditions might also be transmitted via blood components and products, as was the case in rare instances for variant CJD. Recent epidemiological data showing the apparent transmission of haemorrhage risk between blood donors and recipients raise the possibility of blood-based CAA transmission. In this Viewpoint, we review the evidence for amyloid β transmission, provide an overview of relevant prion biology, and consider the circumstances under which bloodborne prion transmission has previously occurred. We discuss the implications for blood transfusion services, particularly in light of the UK Infected Blood Inquiry, and the key questions that need to be addressed to better quantify transfusion-related risk.