Progesterone neuroprotection in traumatic CNS injury and motoneuron degeneration
De Nicola AF et al. – A review summarizes the current understanding of progesterone neuroprotection in traumatic CNS injury and motoneuron degeneration, with a focus on spinal cord injury (SCI). Also discussed are multiple mechanisms contributing to progesterone effects and role of classic nuclear receptors, extra nuclear receptors, membrane receptors, and reduced metabolites of progesterone in neuroprotection and myelin formation. Methods- Review of progesterone neuroprotection in traumatic CNS injury and motoneuron degeneration
Results- Progesterone promotse remyelination, axonal regeneration and recovery of function in peripheral neuropathies
- Progesterone reduces edemas and inflammatory cytokines, prevents neuronal loss, and improves functional outcomes in traumatic brain injury
- Short-and long-term progesterone treatment induces significant improvement in disability level for brain injury pts
- In experimental SCI, impaired molecular markers of functional motoneurons
- Markers: brain-derived neurotrophic factor mRNA, Na,K-ATPase mRNA, microtubule-associated protein 2 and choline acetyltransferase
- SCI produces motoneuron chromatolysis; progesterone treatment restores molecule expression with subsided chromatolysis
- SCI causes oligodendrocyte loss and demyelination
- Short progesterone treatment enhances proliferation and differentiation of oligodendrocyte progenitors into mature myelin-producing cells
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