Neurochemical Aspects of Excitotoxicity

About 40% of central nervous system synapses use glutamate as the neurotransmitter. Over-stimulation of glutamate receptors produces neuronal injury or death by excitotoxicity, which is closely associated with neurochemical and neuropathological changes involved in acute neural trauma (stroke, spinal cord trauma, and head injury) and neurodegenerative diseases such as Alzheimer disease, Parkinson disease, Huntington disease, amyotrophic lateral sclerosis (ALS), Creutzfeldt-Jakob disease, Guam-type amyotrophic lateral sclerosis/Parkinson dementia (ALS/PDC), and multiple sclerosis.

In the past decade, our understanding of the biochemistry, molecular biology, and neuropathology of the glutamate transporters and receptors has exploded. It is becoming increasingly evident that molecular mechanisms, which govern the transfer of the death signal from the neural cell surface to the nucleus, depend on lipid mediators and on cross talk among excitotoxicity, oxidative stress, and neuroinflammation, and that interactions among these three processes play a major role in neuronal cell death during acute neural trauma and neurodegenerative disease. These processes may be primary initiating points in neurodegeneration or they may be the end result of the neurodegenerative process itself.

Neurochemical Aspects of Excitotoxicity provides extensive insight into glutamate transporters and receptors, including their role in the brain with other neurochemical parameters in excitotoxicity, and possible treatments. This book will be of interest scientists already working in the field of excitotoxicity who are interested in gaining a broader understanding of this complicated subject area, as well as graduate students and neurologists who are curious about a common cause of neuronal injury and neurological disorders.