We suspect this may be due to the differing procedures adopted in brain injury and reduced area and density in the corpus callosum after TBI. In addition to these interesting Lapatinib mechanism results observed in the Nogo AB deficient mice, the NgR defi cient mice also display impaired cognitive outcomes in the Morris water maze task after TBI. It has also been reported that Nogo A plays a critical role in stabilizing and maintaining the architecture of hippocampal pyramidal neurons. These results suggest that the role of Nogo A in TBI induced neuronal damage is very complex and may also be age dependent. Brain edema is one of the characteristic features observed in patients suffering from severe traumatic brain injury, and induction. In our model, the TBI induced diffused dam age may not be restricted to neuronal injury.

It might also cause vessel ruptures and severe damage to the blood brain barrier. Consequently, TBI could have accelerated the recruitment of microglia and macro phages, and in turn promptly Inhibitors,Modulators,Libraries stimulated earlier Nogo A expression. The other possible explanation for the varia tions in Nogo A expression profiles may be the specific brain area that was subject to investigation in this study. Based on the results from our previous studies showing that the hippocampus exhibits rather severe neuronal Inhibitors,Modulators,Libraries loss due to TBI, it follows that a more rapid TBI re sponse, including Nogo A upregulation, should be more clearly observed in the hippocampus. The role of Nogo A is controversial.

Using monoclonal antibodies to neutralize Nogo A or using soluble fragments of NgR to block the Nogo A NgR interaction has been found to increase axonal outgrowth and sprouting significantly, which correlates with an im provement of functional outcome Inhibitors,Modulators,Libraries after cerebral ischemia or stroke. Neutralization of Nogo A by mAbs has also been shown to improve cognitive recovery after TBI. These studies suggest that Nogo A elicits the axonal inhibitory effects after injury and provide a po tential treatment strategy for TBI. However, contrary to the pharmacological results, the genetic deletion of Nogo A did not improve functional and histological out comes after TBI in aging animals. Compared with wild littermates, the Nogo AB deficient mice showed diminished recovery from neurological motor deficits it can be classified into vasogenic edema and cytotoxic edema.

Vasogenic edema, a secondary response to BBB compromise following TBI, can lead Inhibitors,Modulators,Libraries to a swelling process and a subsequent rise in intracranial pressure. Cytotoxic edema causes intracellular fluid accumulation Inhibitors,Modulators,Libraries and occurs during water intoxication and under anoxia generating conditions, such as trauma and stroke. Earlier studies have demonstrated that some neuroprotective agents, such as tamoxifen, could protect animals from spinal www.selleckchem.com/products/Sorafenib-Tosylate.html cord injury induced edema and neuronal damage via the attenu ation of Nogo A.