Editorial [Hot Topic: Neurodegeneration and Neuroregeneration:Recent Advancement and Future Perspectives (Executive Editor: H.S. Sharma)

Abstract

Neuroprotection: Non-Neural Cells Regulate Neuronal Functions The term “Neuroprotection” normally denotes rescue of nerve cells. However, the non-neural cells, i.e., glial cells and endothelial cells are equally important for brain function in normal and in pathological conditions [1,2]. The number of glial cells and endothelial cells far exceeds the number of neural cells in the CNS [2,3]. In spite of this fact, most attention is still focused to rescue nerve cells following CNS injuries and the role of non-neural cells in neurodegeneration or neuroprotection is largely ignored. Thus, the term “neuroprotection” is normally misleading as neurons are in the minority in the CNS and their function depends on the survival of non-neural cells and vice versa. To restore the normal function of the CNS by pharmacological manipulation, revival of glial cells and endothelial cell functions are equally important [4-6]. The nerve cell function is largely dependent on the normal endothelial cell and glial function. Thus, it is imperative that in pathological conditions, reducing damage to endothelial cells and/or glial cells by pharmacological agents will improve nerve cell function. Alternatively, glial cells, endothelial cells are all working to maintain and regulate neuronal function in health and disease [7,8]. Taken together, it appears that both the neural and non-neural components of the CNS are working in synergy for maintaining normal brain function and alterations in any neural or non-neural component will have severe impact on CNS structure and function. Blood-Brain vs. Brain Blood Barriers Our CNS is well equipped with the blood-brain barrier that is anatomically located within the endothelial cells of the brain microvasculature [1]. It is assumed that both the luminal and the abluminal cell membranes of the endothelium are equally “tight” to maintain an effective barrier between blood to brain and brain to blood [1,2]. Interestingly, the endothelial cell function and membrane transport from brain to blood (brain-blood barrier) in relation to neurodegeneration and neurorepair mechanisms are still largely ignored [see7,8]. Thus, it is still unclear whether luminal barrier disruption always accompanied with identical damage to the abluminal barrier function. However, there are reasons to believe that when luminal membrane is permeable, the abluminal side is also showing some alteration in the membrane function. A direct evidence to support or reject this hypothesis is still lacking. Studies carried out in our laboratory suggest that hyperthermia induced breakdown of the blood-brain barrier is also associated with a leaky brain blood-barrier [5,9]. Thus, serotonin transport occurs from brain to the blood causing a massive accumulation of the amine in the circulation leading to a generalized and widespread disruption of the blood-brain barrier [9]. This large increase in plasma serotonin is largely prevented by destruction of the serotoninergic neurons into the brain [see 5,9]. This treatment did not allow brain serotonin to increase and thus, the plasma serotonin concentration is much lower resulting in a minor breakdown of the blood-brain barrier in hyperthermia [5]. This suggests that various endogenous substances, e.g., cytokines, growth factors, growth hormone etc. are released from brain in extra quantity following injury that could be transported into the blood stream to have a generalized effect on the cerebral circulation and/or brain function. However, this is entirely a new subject and requires additional investigation in details to achieve better neuroprotection in future. In this volume, the term “Neuroprotection” is employed in its widest sense to include protection of all the “neural” and “nonneural” components of the CNS. This issue highlights the role of non-neural cells; especially the function of endothelial cells and its surrounding glial cells in neurodegeneration and repair process.......