Beta-Amyloid Related Neurodegenerative and Neurovascular Diseases: Potential Implications for Transfusion Medicine

• Cerebral Amyloid Angiopathy (CAA) arises from beta-amyloid deposition in cerebral arteries and arterioles (typically leptomeningeal and cortical), causing recurrent intracerebral hemorrhage (ICH) and dementia. • Converging data suggest prion-like transmissibility of beta-amyloid in humans is possible. • A recent study suggests that recipients of blood transfusions from donors who later develop recurrent ICH, are themselves at greater risk of ICH. • The possibility of transfusion-transmissible CAA raises public health concerns and calls for future research. Cerebral amyloid angiopathy (CAA) is a progressive cerebrovascular and neurodegenerative disorder that is caused by the aberrant accumulation of soluble beta-amyloid isoforms in the small vessel walls of the cerebral and cerebellar cortices and the leptomeninges. Vascular beta-amyloid deposition increases vulnerability to intracerebral hemorrhage (ICH). Clinically, CAA can be the underlying cause of up to half of spontaneous lobar ICHs and can also present with convexity subarachnoid hemorrhage, transient focal neurologic episodes and progressive cognitive decline leading to dementia. The majority of CAA is sporadic, with increasing prevalence with age and often coexists with Alzheimer's Disease (AD). Genetic and iatrogenic etiologies are rare. Cases of CAA and AD have been linked to the use of cadaveric pituitary hormone and later life iatrogenic CAA has also been described following early-life neurosurgical procedures with cadaveric dura grafts. Together these data suggest a capacity of beta-amyloid transmissibility. A recent study found that in over 1 million transfusion recipients from donors who later developed (i) >1 ICH or (ii) one ICH event and dementia, had an elevated risk of developing future ICH. Considering prior reports of transfusion associated variant-Creutzfeldt Jakob Disease in humans and in vivo evidence in sheep, coupled with emerging data supporting beta-amyloid's prion-like properties, raises the question of whether CAA could be transmissible by blood transfusion. This would also have implications for screening, especially in an era of emerging plasma biomarkers of cerebral amyloidosis. Given the public health concerns raised by this biologically plausible question, there is a need for future studies with well-characterized definitions – and temporal ascertainment – of CAA exposure and outcomes to examine whether CAA is transfusion-transmissible, and, if so, with what frequency and timing of onset.

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