Carl Jorns

Amyloid beta (Aβ) associated diseases, such as Alzheimer’s disease and cerebral amyloid angiopathy (CAA), have repeatedly been found to be experimentally transmissible in animals in a prion-like pattern. Recent studies also indicate that such transmission may occur iatrogenically also in routine medical care, following treatment with cadaveric growth hormone, brain surgery and possibly also following blood transfusion. Because diseases in the Aβ-associated spectrum are comparably common, the public health consequences of such transmission may be sizable, especially in organ and ocular tissue transplantation where donors often already have manifest such disease, given that these donors have commonly succumbed to catastrophic intracerebral hemorrhage, one of the hallmark features associated with CAA. Because outcomes following both organ and ocular tissue transplantation in recent years are very good, with large fractions of patients surviving several decades, Aβ transmission could lead to negative patient health effects even considering that incubation times are likely protracted. In this study we will establish a cohort of patients who have undergone solid organ or ocular tissue transplantation, together with data on the medical history of their donors, with the purpose of investigating whether evidence of Aβ proteinopathy in donors leads to an increased risk of Alzheimer’s disease or spontaneous intracerebral hemorrhage in their recipients.