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10.1021/jm400887j 49 HallbergM

Yang Y, Estrada EY, Thompson JF, Liu W, Rosenberg GA (2007) Matrix metalloproteinase-mediated disruption of tight junction proteins in cerebral vessels is reversed by synthetic matrix metalloproteinase inhibitor in focal ischemia in rat

The histopathological hallmark of the cuprizone model as standardized by Hiremath is oligodendrocyte death and subsequent demyelination in the corpus callosum, superior cerebellar peduncles, hippocampus [42, 4654] and several other areas of the mouse brain (reviewed in [20])

The findings suggest that LepR activation is a two-step process wherein leptin first forms a 1:1 complex on the cell membrane with LepR by binding it via the high affinity site 2 interface