By Kewal K. Jain
Neuroprotection has been put on a company clinical foundation prior to now decade as a result of a much better knowing of the molecular foundation of neurological illnesses and the data that therapy of neurological issues shouldn't be in simple terms symptomatic yet preventative opposed to the development of the underlying ailment, in addition to regenerative. The guide of Neuroprotection serves as a entire evaluate of neuroprotection in accordance with wisdom of the molecular foundation of neurological problems. Neuroprotective results of older, validated medications, in addition to new medicinal drugs in improvement, are good documented during this special quantity, that includes the main state-of-the-art and cutting edge tools at present in use.
In-depth and authoritative, The guide of Neuroprotection includes a compendium of significant wisdom aimed toward delivering researchers with an important reference for this key neurological sector of study.
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Additional resources for The Handbook of Neuroprotection
Example text
An isolated rat optic nerve in vitro enables the test conditions to be designed to simulate the environment encountered by an axon during periods of insult, such as transient ischemia and glucose deprivation. Such transient insults trigger progressive axonal degeneration beyond the time at which the insult is removed. This model system allows pharmacological agents to be tested post-insult for their ability to protect against further damage, a scenario most likely to be faced in the clinical setting where patients are not presented until after an event such as a stroke or spinal injury.
Various pharmacological agents were developed to counteract these phenomena. Best known among these were free radical scavengers and anti-excitotoxic agents. 2 and are discussed briefly in the following text. A neurotrophic factor is synthesized by and released from target cells of the neurons bound to specific receptors. It is then internalized and transported by retrograde axonal transport to the cell soma where multiple survival-promoting effects are initiated (Jain 2010a). Neurotrophic factors are discussed in more detail in various chapters dealing with disorders such as stroke and central nervous system (CNS) trauma.
Peripheral sensory neurons depend on galanin for neurite extension after injury, mediated by the activation of the second galanin receptor subtype (GALR2). Galanin has also been shown to act as an endogenous neuroprotective factor to the hippocampus in a number of in vivo and in vitro models of injury (Elliott-Hunt et al. 2004). Less cell death was observed in the hippocampus of galanin-overexpressing transgenic animals after kainate injection and in organotypic cultures after exposure to staurosporine.