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Given the important roles of BBB in the development and progression of various neurological disorders, the BM has been hypothesized to contribute to the pathogenesis of these diseases. After stroke, a cerebrovascular disease caused by rupture (hemorrhagic) or occlusion (ischemic) of cerebral blood vessels, the BM undergoes constant remodeling to modulate disease progression. Although an association between BM dissolution and stroke is observed, how each individual BM component changes after stroke and how these components contribute to stroke pathogenesis are mostly unclear. In this review, I first briefly introduce the composition of the BM in the brain. Next, the functions of the BM and its major components in BBB maintenance under homeostatic conditions are summarized. Furthermore, the roles of the BM and its major components in the pathogenesis of hemorrhagic and ischemic stroke are discussed. Last, unsolved questions and potential future directions are described. 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