New Perspectives of Central Nervous System Injury and Neuroprotection

New Perspectives of Central Nervous System Injury and Neuroprotection, 1st Edition

New Perspectives of Central Nervous System Injury and Neuroprotection, 1st Edition,Hari Shanker Sharma,ISBN9780123869869

International Review of Neurobiology

H Sharma   

Academic Press




229 X 152

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Key Features

  • Reviews written by experts in such a way that provides basic knowledge for beginners and advanced information for researchers and experts
  • New aspects of Neurodegenerative diseases such as; Alzheimer’s Disease, Parkinson’s Disease, Amyotrophic Lateral Sclerosis are presented with the latest therapeutic measures
  • Exacerbation of brain pathology in hypertension or diabetes is discussed for the first time


Central nervous system (CNS) diseases such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis affect a large number of populations worldwide for which no suitable cure is currently available. In addition, stroke, nanoparticle intoxication, diabetes, hypertension, and psychostimulant abuse either alone or in combination are capable of inducing potential brain damage. Thus, there is an urgent need to expand our knowledge to find suitable therapeutic strategies to enhance neurorepair processes in such diseases.

This volume presents neuroprotection and novel therapeutic strategies developed in the last 5 years by 12 world leaders in the field. The term neuroprotection means rescuing neuronal and non-neuronal cells together. The cerebral endothelium that constitutes the anatomical and physiological site of the blood-brain barrier (BBB) is one of the most important non-neural cells in the CNS. Any distortion of the BBB leads to brain diseases and restoration of the barrier results in neuroprotection. Thus, the BBB appears to be the "gateway" for neurological diseases and neurorepair. However, to treat brain tumors or infarcts, new therapeutic strategies are needed to enhance brain drug delivery using nanotechnology. In addition, apart from conventional drugs, restoration of BBB function could also be achieved by means of antibodies directed against specific proteins, neurotransmitters or exogenous supplement of neurotrophic factors. Since co-morbidity factors e.g., hypertension, diabetes, and exposure of nanoparticles could complicate the pathogenesis of neurological disorders either an enhanced dose of the drug or nanodelivery of a combination of several drugs is needed to achieve neuroprotection.

This volume of International Review of Neurobiology is the first to discuss novel therapeutic strategies in situations of neurological disorders in combination with different co-morbidity factors.


Neuroscientists, neurologists, psychologists

Information about this author is currently not available.

New Perspectives of Central Nervous System Injury and Neuroprotection, 1st Edition

  • Series Page
  • Contributors
  • Preface
  • Acknowledgments
  • Chapter 1 The Function and Mechanisms of Nurr1 Action in Midbrain Dopaminergic Neurons, from Development and Maintenance to Survival
    • I Introduction
    • II The Midbrain Dopamine System: Neurochemistry
    • III The Midbrain Dopamine System: Development
    • IV Dopaminergic Neurons and Parkinson’s Disease
    • V Nurr1, A Protein Whose Function Is Important in the Life Cycle of VM DANs
    • VI The Mechanisms of Nurr1 as a Nuclear Receptor
    • VII Most Recent Development in Application of Nurr1 in Dopaminergic Differentiation and Implications in Future Treatment for PD
  • Chapter 2 Monoclonal Antibodies as Novel Neurotherapeutic Agents in CNS Injury and Repair
    • I Introduction
    • II Historical Perspectives on the Use of Antibodies as Therapy
    • III Therapeutic Basis of Antibodies
    • IV Antibodies Versus Receptor Antagonist Drugs
    • V Antibodies Neutralize Effects of Endogenous Antigens
    • VI Our Investigations on Monoclonal Antibodies to Induce Neuroprotection in CNS Injuries
    • VII Neuroprotective Effects of Serotonin Antibodies in CNS Injuries
    • VIII Neuroprotection by Dynorphin A Antibodies in CNS Injuries
    • IX Antibodies to nNOS Is Neuroprotective in CNS Injuries
    • X TNF-a Antibodies Are Neuroprotective in CNS Injuries
    • XI Combination of nNOS and TNF-a Antibodies Enhances Neuroprotection in SCI
    • XII Conclusion and Future Perspectives
  • Chapter 3 The Blood–Brain Barrier in Alzheimer’s Disease
    • I Introduction
    • II Pathology of AD
    • III A Receptor-Mediated Transport of apoJ and ABP at the BBB and BCSF-B
    • IV Human Receptors for ABP1-40
    • V Clearance of AB1-40 P from Brain LDL Receptor at the BBB
    • VI Clearance of ABP1-40 in Monkey Model
    • VII Point Mutation of Codon 22 Reduces Clearance of ABP1-40 from the CSF and Prevents Transport from CNS to Blood
    • VIII Circulating ABP Crosses the BBB in Aged Monkeys
    • IX Cerebrovascular Pathology in AD
    • X Existing Theories Regarding Origin of ABP
    • XI Conclusion
  • Chapter 4 Neurovascular Aspects of Amyotrophic Lateral Sclerosis
    • I Introduction
    • II BBB/BSCB Impairment in ALS
    • III Future Perspectives
    • IV Conclusion
  • Chapter 5 Quercetin in Hypoxia-Induced Oxidative Stress: Novel Target for Neuroprotection
    • I Introduction
    • II Hypoxia and Free Radical Generation
    • III Brain: Target to Free Radical Damage
    • IV Antioxidant Defense System
    • V Antioxidant Defense System and Hypoxia
    • VI Pathophysiological Changes in Brain in Response to Hypoxia
    • VII Antioxidant Therapy
    • VIII Our Investigation on Neuroprotection Elicited by Quercetin
    • X General Conclusion and Future Perspective
  • Chapter 6 Environmental Conditions Modulate Neurotoxic Effects of Psychomotor Stimulant Drugs of Abuse
    • I Introduction
    • II Brain Temperature Responses to METH and MDMA are Modulated by Activity State and Environmental Conditions
    • III Adverse Environmental Conditions Enhance Histochemical and Morphological Perturbations Induced by METH: Role of Brain Temperature
    • IV Temperature Modulation of BBB Permeability
    • V Conclusions and Perspectives
  • Chapter 7 Central Nervous Tissue Damage after Hypoxia and Reperfusion in Conjunction with Cardiac Arrest and Cardiopulmonary Resuscitation
    • I Introduction
  • Chapter 8 Interactions Between Opioids and Anabolic Androgenic Steroids: Implications for the Development of Addictive Behavior
    • I Introduction
    • II AAS May Lead to Opioid Dependence
    • III Interactions Between AAS and the Endogenous Opioids
    • IV AAS Dependence Involve Opioid Mechanisms
    • V Conclusions
  • Chapter 9 Neurotrophic Factors and Neurodegenerative Diseases
    • I Introduction
    • II NTFs and Neurodegenerative Diseases
    • III NTF Delivery Approaches: Evolution in Therapies
    • IV Conclusion
  • Chapter 10 Neuroprotective Effects of Cerebrolysin, A Combination of Different Active Fragments of Neurotrophic Factors And Peptides on the Whole Body Hyperthermia-Induced Neurotoxicity
    • I Introduction
    • II Blood–Brain Barrier—A Gateway to Brain Diseases
    • III Factors Affecting Hyperthermia-Induced Brain Damage
    • IV Cerebrolysin, a Novel Therapeutic Agent in Hyperthermia-Induced Neurotoxicity
    • V Functional Significance of These Findings
    • VI Conclusions
    • VII Future Perspectives
  • Chapter 11 Alzheimer’s Disease and Amyloid: Culprit or Coincidence?
    • I Introduction
    • II Amyloid and AD
    • III Tau and AD
    • IV AD and Tau: A Double Act?
    • V White Matter Pathology and AD
    • VI Transgenic Animal Models for AD: What Have They Taught Us?
    • VII Oxidative Stress and AD
    • VIII Inflammation and AD
    • IX Other Amyloid-Independent Mechanisms in AD
    • X Future Perspectives
  • Chapter 12 Vascular Endothelial Growth Factor and Other Angioglioneurins
    • I Introduction
    • II VEGF
    • III Other Angioglioneurins
    • IV Potential Role of VEGF and Other Angioglioneurins in Brain Restoration
    • V Conclusions
  • Subject Index
  • Contents of Recent Volumes

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