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The discovery that the synthetic compound MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) is a substrate of MAOB, which converts this compound to the neurotoxin MPP + (1-methyl-4-phenylpyridinium), causing a parkinsonism syndrome in some mouse strains and primates including humans, provided a basis for our understanding of the participation of MAO in dopaminergic neurodegeneration, and MAOB inhibitors as neuroprotective drugs with disease-modifying activity

reported that vigorous exercise in human subjects increases glutamine levels within the cortex, an effect that occurs as a consequence of activity-dependent increases in the glutamateglutamine turnover (Reference Maddock, Casazza and Buonocore66)

The prohibition of efflux transporters selectively hinders the transport of therapeutic drugs to BBB

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To optimize targeted delivery methods and gene therapy strategies for clinical translation, more studies are necessary

doi: 10.1038/nsmb1222, 108 SatoT.ShapiroJ