The goal of this text is to focus readers attention on three major areas; the origin and localization of GSH in the nervous system; the multiple effects of GSH on neural health activity; and the potential for alterations on GSH status to lead to neurological damage of the type observed in amyotrophic lateral sclerosis, Parkinson's disease and other neurological disorders. The text also touches upon the additional roles of the antoxidant GSH, including possible neurotransmitter action, redox modulation of ionotropic receptor function, and neuroprotection against exicitoxic actions of glutamate.

The function and physiology of the central nervous system (CNS) can be affected by of bacterial, fungal, protozoan, and viral infections. The neurological effects of viruses are associated with direct infections of structures of the CNS, the migration of infected leukocytes to the CNS, or/and the immune response to control the infection. In all these situations, we have reactive oxygen species (ROS) generation. ROS induces several cellular effects, including cell cycle progression, apoptosis, DNA damage, senescence, and neurodegeneration. The control of ROS involves the glutathione (GSH) balance, owing to antioxidant activity. Moreover, GSH is related with the transport of endogenous/exogenous molecules to extracellular medium by ABCC1/MRP1 activity. The depletion of GSH levels characterizes viral infections and associated-disease progression. Many studies correlated the GSH levels with immune response and suggest adding the glutathione replenishment to highly active antiviral treatment. Thus, it is important to review the relationship between the CNS, immune response, and GSH levels during neurological viral diseases.

"This volume deals with the role of amino acids and small peptides in the central nervous system. The various chapters describe individually the metabolism and functions of the different compounds."--Pref.

Reduced glutathione (GSH) is the most important thiol in living organisms. It is the key component of antioxidant system and serves as a free radical scavenger. There is a cycle of GSH in biological systems and this cycle provides higher intracellular levels of GSH. GSH depletion and apparent oxidative stress may cause toxicity and can affect the general well-being of the organism. GSH was shown to be preventive against aging, cancer, heart disease, infections and dementia. This book is mainly focused on GSH in health and disease. The readers will gain qualified scientific knowledge on the diverse functions of GSH, the importance of GSH status against oxidative stress and the interaction between GSH and nervous system-related infections from this book.

The goal of this text is to focus readers attention on three major areas; the origin and localization of GSH in the nervous system; the multiple effects of GSH on neural health activity; and the potential for alterations on GSH status to lead to neurological damage of the type observed in amyotrophic lateral sclerosis, Parkinson's disease and other neurological disorders. The text also touches upon the additional roles of the antoxidant GSH, including possible neurotransmitter action, redox modulation of ionotropic receptor function, and neuroprotection against exicitoxic actions of glutamate.

The imbalance between the production of reactive oxygen species (ROS) and antioxidant defenses determines a state known as oxidative stress. Higher levels of pro-oxidants compared to antioxidant defenses may generate oxidative damage, which, in turn, may lead to modifications in cellular proteins, lipids, and DNA, reducing functional capacity and increasing the risk of diseases. Nevertheless, the clearance of harmful reactive chemical species is achieved by the antioxidant defense systems. These protection systems are referred to as the first and second lines of defense and comprise the classic antioxidants, enzymatic and nonenzymatic defenses, including glutathione. This book presents and discusses the advancement of research on health and diseases and their underlying mechanisms, exploring mainly aspects related to the glutathione antioxidant system.

Neurodegenerative diseases are characterized by the progressive deterioration of neuronal function in the central or peripheral nervous system and ultimately the death of nerve cells. There is a big evidence that oxidative stress is an essential mediator implicated in neurodegenerative processes and may be a key event triggering various forms of cell death. Here, we review the hypothesis that neuronal loss resulted from oxidative stress may be initiated by a drastic decrease in the antioxidant molecule glutathione (GSH). The impairment of physiological glutathione\¬¥s levels and the alterations in the activities of its related enzymes in neuronal cells are increasingly suggested to be implicated in the initiation and progression of neurodegenerative diseases. GSH plays a vital role in cellular redox homeostasis in the nervous system and protects neurons against a variety of oxidative insults. GSH depletion can enhance oxidative stress and may increase protein aggregation leading to initiate cell death in distinct neuronal populations. Evidence demonstrates a grand impact of oxidative stress and loss neuronal GSH in Parkinson,Äôs disease and Alzheimer,Äôs disease.