Development of new therapies for vascular dementia

血脑屏障（BBB）功能障碍的血管中骨桥蛋白、CD36和LDL受体（LDLR）的表达增加。我们可以生产骨桥蛋白的合成肽、骨桥蛋白的抗体、表达骨桥蛋白的病毒载体。高血压大鼠和快速老化小鼠脑内BBB功能障碍血管中CD 36表达增加。诱导CD36或LDLR表达降低的药物可能有助于血管性痴呆的治疗。此外，血管紧张素受体阻滞剂（ARB）可减少血管损伤，包括BBB损伤，这表明ARB与骨桥蛋白联合使用可能对血管性痴呆的治疗有效。

The expression of osteopontin, CD36, and LDL receptor (LDLR) was turned out to be increased in vessels showing blood-brain barrier (BBB) dysfunction. We could productsynthetic peptides of osteopontin, an antibody for osteopontin, virus vector expressing osteopontin. The expression of CD36 was turned out to be increased in the vessels showing BBB dysfunction in brains of hypertensive rats and senescence accelerated mice. Drugs inducing the reduction of CD36 or LDLR expression may be useful for the therapy against vascular dementia. In addition, angiotensin receptor blockers (ARBs) reduced vascular damage including the BBB damage, suggesting that the usage of ARBs with osteopontin may be effective for the therapy against vascular dementia.