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J. Neurochem. (2010) 113, 930–942. Granulocyte-colony stimulating factor (G-CSF) is a potent hematopoietic factor that drives differentiation of neutrophilic granulocytes. We have recently shown that G-CSF also acts as a neuronal growth factor, protects neurons in vitro and in vivo, and has regenerative potential in various neurological disease models. Spinal cord injury (SCI) following trauma or secondary to skeletal instability is a terrible condition with no effective therapies available at present. In this study, we show that the G-CSF receptor is up-regulated upon experimental SCI and that G-CSF improves functional outcome in a partial dissection model of SCI. G-CSF significantly decreases apoptosis in an experimental partial spinal transsection model in the mouse and increases expression of the anti-apoptotic G-CSF target gene Bcl-XL. In vitro, G-CSF enhances neurite outgrowth and branching capacity of hippocampal neurons. In vivo, G-CSF treatment results in improved functional connectivity of the injured spinal cord as measured by Mn2+-enhanced MRI. G-CSF also increased length of the dorsal corticospinal tract and density of serotonergic fibers cranial to the lesion center. Mice treated systemically with G-CSF as well as transgenic mice over-expressing G-CSF in the CNS exhibit a strong improvement in functional outcome as measured by the BBB score and gridwalk analysis. We show that G-CSF improves outcome after experimental SCI by counteracting apoptosis, and enhancing connectivity in the injured spinal cord. We conclude that G-CSF constitutes a promising and feasible new therapy option for SCI. [ABSTRACT FROM AUTHOR]

The article presents an abstract of the research paper "Mechanisms of Gene Regulation by NF-B and Stress in the Central Nervous System." Cumulative oxidative damage may lead to increased apoptosis. This may be due to chronic exposure to the reactive oxygen species byproducts of oxidative metabolism and neurotransmitter signaling pathways.

The article presents an abstract of a research paper concerning the effect of NF-kB, an acute phase response factor, in genetic regulation of the central nervous system (CNS). NF-kB is sensitive to oxidative stress and has anti-apoptotic and choline acetyl transferase (ChAT) suppressing properties in the CNS. There are alterations in NF-kB-binding activity in aged brain and that the ChAT and Bcl-x genes have NF-kB sites in the promoters that acts as a suppressor and enhancer respectively.

The article presents an abstract of the paper titled "MAP-Kinase and PI-3-Kinase As Transducers of Antiapoptotic BDNF Signaling in CNS Neurons." It investigates the role of neurotrophins MAP-Kinase and PI-3-Kinase in promoting the survival and suppressing apoptosis in the central nervous system neurons.