By Kewal K. Jain
Neuroprotection has been put on an organization medical foundation prior to now decade as a result of a more robust knowing of the molecular foundation of neurological illnesses and the information that therapy of neurological problems shouldn't be only symptomatic yet preventative opposed to the development of the underlying sickness, in addition to regenerative. The guide of Neuroprotection serves as a finished evaluation of neuroprotection in keeping with wisdom of the molecular foundation of neurological issues. Neuroprotective results of older, proven medicinal drugs, in addition to new medicines in improvement, are good documented during this certain quantity, that includes the main state of the art and leading edge equipment at present in use.
In-depth and authoritative, The guide of Neuroprotection includes a compendium of significant wisdom geared toward supplying researchers with an important reference for this key neurological quarter of study.
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Additional resources for The Handbook of Neuroprotection
Gene/protein response to ischemia/injury includes c-fos/jun, hsp70, TGF-b1, NGF, and FGF. Within minutes of an insult, there is increased production of fos/jun, which may be triggered by stimulation of glutamate NMDA receptors, changes in cAMP, or increases in intracellular calcium. The effect may be translated into hsp, which act as molecular chaperones and have a neuroprotective function. Several gene expression databases contain information on large-scale analysis of genes that are involved in neurotrauma, and neuronal differentiation and regeneration.
Brain imaging provides important biomarkers of neurological disorders that can be used for diagnosis and monitoring treatment effects in clinical trials (Jain 2010b). Brain imaging findings, combined with clinical correlations, can be used as surrogate biomarkers of response even for the later stages of drug development. Technological advances in imaging have made it possible to extract information noninvasively from the human brain regarding a drug’s mechanism and site of action. The tools include PET, SPECT, CT, and functional magnetic resonance imaging (fMRI).
2009). Minute-by-minute monitoring revealed no detectable volume regulation during these osmotic challenges, particularly during the first 5 min. Astrocytes also rapidly swell in response to oxygen/glucose deprivation for 10 min, but astroglial volume recovers quickly when slices are re-supplied with oxygen and glucose, while neurons remain swollen. In vivo, rapid astroglial swelling is confirmed within 6 min following intraperitoneal water injection or during the 6–12 min following induced cardiac arrest in rats.