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, aswell as graduate students and
neurologists who are curious about a common cause of neuronal
injury and neurological disorders.
General
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