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Whole genome expression of cellular response to stroke.

Many attempts have been made at developing biomarkers for stroke. Although successful to some degree,1–3 none have been sufficiently robust to be used in clinical practice. Thus, there is still a great need for more in-depth studies of the biology of human stroke to understand its pathogenesis better. This should make it possible to develop blood tests for stroke and transient ischemic attacks (TIAs) to guide treatment and ultimately improve outcomes.

The traditional approach to develop stroke biomarkers has been to select candidate markers based on known pathobiology. The majority of markers that have been evaluated are proteins that are measured in patients at various times before or after stroke. The rationale for this approach is that brain injury releases molecules into blood that can be measured as evidence of brain injury; or that other cells and organs release molecules that either cause or contribute to a stroke, or are a response to the stroke. These approaches have been handicapped because they require a guess at the most reliable biomarker.

Our group took a different approach to the problem by assessing the immune system after stroke.4,5 The rationale for this approach is shown in Figure 1. The expression of genes in leukocytes is influenced by many factors associated with ischemic stroke. Leukocytes interact with blood clots, platelets, atherosclerotic plaque, and injured brain endothelial cells via adhesion molecules.5 In addition, leukocytes detect circulating cytokines, chemokines, and hormones. Each has the potential to modulate RNA expression in leukocytes.



Figure 1. 
Schematic of interactions between circulating leukocytes and factors involved in ischemic stroke, including blood clots, platelets, atherosclerotic plaque, and damaged endothelial cells. Each factor can influence expression of leukocyte RNA. This figure is reproduced from an article by Sharp et al.5



To provide proof-of-principle that …