Repairing the blood-brain barrier

Abstract

Specialized vasculature within the brain forms a blood-brain barrier (BBB) that excludes cellular and soluble plasma contents from the inner workings of the central nervous system (CNS) (1). Stroke, neurodegenerative disease, and brain tumors result in a loss of BBB properties, which contributes to pathology, arguing for therapeutic approaches to restore BBB functions. Conversely, the BBB poses a problem for drug accessibility. Modulating barrier function can enhance and broaden the effectiveness of therapeutic agents on the CNS (2). Development and maintenance of the BBB is regulated by two Wnt ligands, Wnt7a and Wnt7b (3). On page 737 of this issue, Martin et al. (4) describe an elegant molecular dissection of Wnt7 signaling, demonstrating that a single amino acid change in Wnt7a markedly increases its specificity for vascular endothelial cells, resulting in improved outcomes in zebrafish and mouse models of disrupted BBB in tumor growth and stroke.

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