Cerebral amyloid-β (Aβ) angiopathy (CAA) is defined by the aggregation of the protein amyloid-β (Aβ) within the brain’s blood vessels. CAA is common in Alzheimer’s disease (AD) and can cause side-effects when patients receive new anti-Aβ immunotherapies. Currently, there are no specific tests or therapeutics for CAA; therefore, their development would improve personalised treatment. Our research recently revealed that the protein medin is only found in vascular Aβ aggregates (i.e. CAA); that removing medin significantly reduces CAA in mouse models; and that levels of the medin precursor protein, MFG-E8, are lower in the cerebrospinal fluid (CSF) of a subgroup of AD patients with vascular pathology. This suggests that medin could be a new target for treatment and a diagnostic biomarker for CAA, but we need to study this further. Therefore, our consortium’s goals are: 1) to test if removing medin reduces vascular damage in mice receiving Aβ immunotherapy, 2) to assess how changes in MFG-E8 and/or medin levels in the CSF relate to CAA in both mouse models and AD patients, 3) to generate tests for measuring medin, 4) to use these tests to categorise about 1,500 patients based on their CSF profiles, and 5) to compare these results with established radiological markers of CAA. Thus, we will test if biofluid markers of medin can predict CAA pathology, progression and cognitive decline and establish if medin is a new target for diagnosis and treatment of CAA, moving towards more personalised medicine for Alzheimer’s patients.