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The knowledge about functional expression of transporters at the BBB and structural requirements for substrate binding and translocation via the transporters gives tempting opportunity for rational design and development of drugs, prodrugs and nanocarriers, which can utilize the specific BBB transporter for brain delivery of CNS drugs (71, 72)

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In contrast, QA promotes glutamate release in rodent synaptosomes, inhibits astrocytic glutamate uptake, and reduces glutamine synthase activity [83,84,85]

Therefore, investigation of the mechanisms behind such possible changes should be a research priority for future clinical trials