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Although programmed cell death receptor 1 (PD\u20101) mediates neurogenesis, its role in cerebrovascular development remains poorly understood. Here, a correlation between cerebral vessels and oligodendrocyte precursor cells (OPCs) is revealed during brain development. The ablation of endothelial PD\u20101 triggers cortical hypervascularization through excessive angiogenic sprouting, concomitantly driving OPC differentiation. These alterations disrupt blood brain barrier (BBB) maturation, induce dysmyelination, and ultimately result in abnormal behavior in mice. Mechanistically, the loss of endothelial PD\u20101 suppresses the activity of the Wnt\/\u03b2\u2010catenin signaling pathway, thereby disrupting normal angiogenesis. Concurrently, it activates the MEK1\/2\u2010ERK1\/2\u2010GLI1 pathway, leading to increased GREMLIN1 (GREM1) expression. Elevated GREM1 secretion inhibits the BMP\/SMAD1\/5\/SMAD4 signaling cascade in OPCs, which inhibits oligodendrogenesis and myelination. 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