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Article
Open AccessNeuroprotection by eIF2α-CHOP inhibition and XBP-1 activation in EAE/optic neuritiss
No therapies exist to prevent neuronal deficits in multiple sclerosis (MS), because the molecular mechanism responsible for the progressive neurodegeneration is unknown. We previously showed that axon injury-i...
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Article
Open AccessAKT-dependent and -independent pathways mediate PTEN deletion-induced CNS axon regeneration
Phosphatase and tensin homolog (PTEN) acts as a brake for the phosphatidylinositol 3-kinase–AKT–mTOR complex 1 (mTORC1) pathway, the deletion of which promotes potent central nervous system (CNS) axon regenera...