Oxidative Damage in Neurological Dysfunction/Diseases: Causes and Prevention

Dear Colleagues,

Oxidative/nitrosative stress are major contributors to neurological damage and central nervous system diseases. Its high vulnerability stems in part from is elevated requirement for glucose and oxygen; the brain utilizes 20% of the inhaled oxygen even though it is only 2% of the body weight. Any reduction in the oxygen tension in neurons is accompanied by rapid changes in mitochondrial metabolism and ATP production, which is needed to sustain optimal neuronal physiology. These changes exaggerate reactive oxygen species production due to malfunction of the electron transport chain and the activation of cellular oxidases These destructive agents mutilate critical molecules generically-referred to as oxidative stress; this culminates in apoptosis, autophagy, mitophagy, etc. Loss of neurons is particularly serious since, with few exceptions, neurons are not replaced. Numerous attempts and agents have been tested in recent years relative to their ability to attenuate neural damage that occurs as a result of oxygen deprivation, toxin exposure, or as a result of disease processes. The molecules tested include endogenously-produced agents, e.g., melatonin, as well as vitamins and many other plant-derived, naturally-occurring agents as well as synthetic pharmaceutical drugs. The ability to modulate and/or delay diseases processes in the central nervous system is a high priority considering the increased longevity of humans. Old age is a major predisposing factor for the elevated likelihood of the development of neurological impairment. The intent of this special issue is to assemble the published information which describe the causes of neurological damage/diseases as well as data related to the preservation of neural and cognitive functions throughout life.

Prof. Russel J Reiter and Assoc. Prof. Ramaswamy Sharma

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