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This open access book presents the roles and mechanisms of signal
transduction triggered by nicotinic acetylcholine receptors
(nAChRs) stimulation in neuroprotection against toxic effects of
risk factors of neurodegenerative diseases. Accumulating evidence
suggests that nAChRs in the CNS play important roles not only in
excitatory neurotransmission but also in neuronal survival and
related functions. Neuroprotection mediated by nAChRs in
neurodegenerative diseases such as Alzheimer's disease is the major
topic of this book. In response to rapidly evolving areas in
clinical and laboratory neuropharmacology and neurochemistry, this
volume provides in-depth coverage of neuroprotection in basic
research and future developments in the clinical application of
effective neuroprotective strategies in neurodegenerative diseases.
This work appeals to both basic and clinical researchers in several
fields, such as neuroscience, neurology, and pharmacology.
New research suggests it is highly probable that DOPA, in addition
to being a precursor to dopamine, functions by itself as a
neurotramsmitter and/or neuromodulator. Neurobiology of DOPA as a
Neurotransmitter integrates background information about DOPA as an
inert amino acid precursor of dopamine with the evidence showing
that DOPA fulfills several criteria of neurotransmitters. Providing
easy access to, and complete understanding of, the latest research
on the subject, the book makes the case that DOPA meets many of the
criteria of neurotransmitters and includes anti-evidence in some
instances. The book begins with a historical review of current
knowledge of DOPA. It characterizes DOPA as a prominent example
showing transmutation from an inert substance to a gold drug in
Parkinson's disease and further to a neurotransmitter in its own
right. The next chapters cover the essential criteria of a
neurotransmitter such as synthesis, existence, and competitive
antagonism. The book describes metabolism composed of catecholamine
synthesis and degradation products related to neuron death,
physiological release of DOPA in the lower brainstem, striatum, and
nucleus accumbens, and physiological or pharmacological responses
involved in baroreflex neurotransmission and related to behavioral
science including interactions with catecholamines, acetylcholine,
glutamate, and GABA. The book explores recognition sites, transport
sites, and therapeutic role and mechanisms for neuron death related
to adverse influence in the treatment of Parkinson's Disease.
Edited by experts in the field, the breadth and depth of
information contained in this book is confirmed by a quick scan of
the chapter authors. Theysummarize the issues surrounding DOPA
neurotoxicity and explore the link between experimental studies and
clinical relevance.
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