Alzheimer’s disease is the most common cause of dementia. It is characterised by the clumping of amyloid and tau proteins in the brain, which leads to a decline in thinking skills. People with Alzheimer’s disease, however, vary greatly in rates of decline and in underlying pathophysiology. Such differences between individuals with Alzheimer’s disease hampers the search for cures. We recently discovered five biological variants of Alzheimer’s disease based on large scale protein measurements in the cerebrospinal fluid. Each biological variant was related to different underlying causes of Alzheimer’s disease. For example, one variant was characterised by inflammation. Another variant was characterised by leakage of the blood-brain barrier. It is likely that each biological variant will need its own treatment. To develop such personalised treatment approaches, easy to obtain markers are needed that can help to identify which biological variant a person with Alzheimer’s disease has. While cerebrospinal fluid is in close contact with the brain, and provides an accurate reflection of ongoing disease processes, it requires a lumbar puncture. Blood is easier to collect, and previous research has demonstrated that the Alzheimer’s disease proteins amyloid and tau can be accurately detected in blood. However, these two proteins cannot distinguish between biological variants in Alzheimer’s disease. We hypothesise that a subset of other protein markers exists in the blood that can distinguish biological variants of Alzheimer’s disease. Technological advances now make it possible to measure the levels of thousands of other proteins in the blood. In this project we will make use of these technologies to identify the most optimal subset of markers in blood for each the five biological variants of Alzheimer’s disease.  Our project will be the first step towards precision medicine in Alzheimer’s disease, by removing barriers to apply such subtyping in clinical trials.