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International Review of Neurobiology, Volume 42 [Hardback]

Volume editor (University of Texas, Austin, U.S.A.), Volume editor (Emeritus Professor of Pharmacology, Institute of Pharmaceutical Sciences, Kings College London, London, UK), Volume editor (Louisiana State University Medical Center, School of Medicine, Baton Rouge, U.S.A.)
  • Formāts: Hardback, 345 pages, height x width: 229x152 mm, weight: 620 g
  • Sērija : International Review of Neurobiology
  • Izdošanas datums: 09-Feb-1998
  • Izdevniecība: Academic Press Inc
  • ISBN-10: 0123668425
  • ISBN-13: 9780123668424
Citas grāmatas par šo tēmu:
  • Formāts: Hardback, 345 pages, height x width: 229x152 mm, weight: 620 g
  • Sērija : International Review of Neurobiology
  • Izdošanas datums: 09-Feb-1998
  • Izdevniecība: Academic Press Inc
  • ISBN-10: 0123668425
  • ISBN-13: 9780123668424
Citas grāmatas par šo tēmu:
The latest issue offers seven studies. They cover Alzheimer's disease; the neurobiology of stroke; free radicals, calcium, and the synaptic plasticity-cell death continuum; AP-1 transcription factors: short-term and long-term modulators of gene expression in the brain; ion channels in epilepsy; post-translational regulation of ionotropic glutamate receptors and synaptic plasticity; and new insights into the ligand-gated ion channel receptor superfamily provided by heritable mutations in various receptors. Annotation c. by Book News, Inc., Portland, Or.

Volume 42 presents an in-depth review on Alzheimer's Disease as well as a look at several transcription factors.

Key Features
* Clinical features of stroke and the current stasis of stroke therapy
* Alzheimers Disease--pathology, pathological proteins, etiology, pathogenesis, neurotransmitter alterations, and treatment strategies
* An examination of the regulation of AP-1 and related transcription factors and their role in brain injury and drug abuse-related behavior
* Emerging roles of the transcription factor NF(B
* Recent advances about the nature of alterations in ion channel structure or function which may be responsible for epileptogenesis
* An integrated model accounting for the multiple mechanisms involved in the posttranslational regulation of glutamate ionotroic receptors
* Genetic mutation and the Glycine Receptor

Papildus informācija

Key Features * Clinical features of stroke and the current stasis of stroke therapy * Alzheimers Disease--pathology, pathological proteins, etiology, pathogenesis, neurotransmitter alterations, and treatment strategies * An examination of the regulation of AP-1 and related transcription factors and their role in brain injury and drug abuse-related behavior * Emerging roles of the transcription factor NF(B * Recent advances about the nature of alterations in ion channel structure or function which may be responsible for epileptogenesis * An integrated model accounting for the multiple mechanisms involved in the posttranslational regulation of glutamate ionotroic receptors * Genetic mutation and the Glycine Receptor
CONTRIBUTORS ix Alzheimer Disease 1(55) MARK A. SMITH I. The Disease and Diagnosis 1(2) II. Pathology 3(13) III. Pathological Proteins 16(9) IV. Etiology 25(7) V. Pathogenesis 32(5) VI. Neurotransmitter Alterations 37(1) VII. Treatment Strategies 38(1) VIII. Future Developments and Research Avenues 39(1) References 40(16) Neurobiology of Stroke 56(47) W. DALTON DIETRICH I. Introduction 56(1) II. Classification of Strokes 56(1) III. Incidence and Risk Factors 57(2) IV. Stroke Prevention 59(1) V. Animal Models of Cerebral Ischemia and Stroke 60(8) VI. Factors Regulating Ischemic Outcome 68(3) VII. Pathophysiology of Ischemic Neuronal Damage 71(5) VIII. Neuroprotection 76(5) IX. Clinical Trials of Stroke 81(4) X. Conclusions and Future Directions 85(1) References 86(17) Free Radicals, Calcium, and the Synaptic Plasticity-Cell Death Continuum: Emerging Roles of the Transcription Factor NF (k)B 103(66) MARK P. MATTSON I. Introduction 103(6) II. Roles of Calcium and Free Radicals in Signaling at Growth Cones and Synapses 109(20) III. Emerging Roles of NF (k)B in Neuronal Plasticity 129(3) IV. Roles of Calcium and Free Radicals in Synaptic Degeneration and Cell Death 132(12) V. Programmed Cell Life and the Evolution of Calcium and Free Radical Signaling at Growth Cones and Synapses 144(11) VI. Emerging Roles of NF (k)B in Cytoprotection and Apoptosis 155(4) VII. Conclusions 159(2) References 161(8) AP-1 Transcription Factors: Short- and Long-Term Modulators of Gene Expression in the Brain 169(30) KEITH PENNYPACKER I. Introduction 169(2) II. AP-1 and Related Proteins 171(2) III. Regulation 173(10) IV. Neurodegeneration 183(4) V. Drug Abuse 187(4) VI. Conclusions: AP-1 Proteins as Pharmacological Targets 191(1) References 192(7) Ion Channels in Epilepsy 199(28) ISTVAN MODY I. Introduction 199(1) II. Plasticity of Ion Channels and Experimental Models of Epilepsy 200(2) III. Ligand-Gated Ion Channels 202(11) IV. Voltage-Gated Ion Channels 213(3) V. Summary and Conclusions 216(1) References 217(10) Posttranslational Regulation of Ionotropic Glutamate Receptors and Synaptic Plasticity 227(58) XIAONING BI STEVE STANDLEY MICHEL BAUDRY I. Introduction 227(4) II. Characterization of Ionotropic Glutamate Receptors 231(11) III. Regulation of Glutamate Receptors by Phosphorylation 242(4) IV. Regulation of Glutamate Receptor Properties by Calpains 246(2) V. Regulation of AMPA Receptors by Phospholipases and Phospholipids 248(2) VI. Targeting and Anchoring of Glutamate Receptors 250(6) VII. Turnover of Glutamate Receptors 256(5) VIII. Links between Glutamate Receptor Regulation and Synaptic Plasticity 261(8) IX. Concluding Remarks 269(1) References 270(15) Heritable Mutations in the Glycine, GABA(A), and Nicotinic Acetylcholine Receptors Provide New Insights into the Ligand-Gated Ion Channel Receptor Superfamily 285(48) BEHNAZ VAFA PETER R. SCHOFIELD I. Introduction 285(2) II. The Ligand-Gated Ion Channel Receptor Superfamily 287(4) III. The Four-Loop Model of Ligand Binding 291(8) IV. The Ion Channel 299(7) V. Heritable Defects of LGIC Receptors 306(19) VI. Future Directions 325(2) References 327(6) INDEX 333(8) CONTENTS OF RECENT VOLUMES 341
Professor Peter Jenner is a specialist in preclinical aspects of neurodegenerative diseases, notably Parkinsons disease. He has spent the major part of his career at Kings College London where he was Head of Pharmacology for 14 years before returning to his research roots and subsequently becoming Emeritus Professor of Pharmacology. Peter has expertise in drug metabolism and pharmacokinetics but neuropharmacology based on functional models of neurodegenerative diseases has formed the major focus of his work. Peter holds a BPharm, PhD and DSc degree from the University of London. He has published well over 1000 articles with more than 700 peer reviewed papers. He is a Fellow of the Royal Pharmaceutical Society, the British Pharmacological Society, the Royal Society of Medicine and of Kings College London. Peter was recently honoured with a Doctor Honoris Causa degree from Carol Davila University of Medicine and Pharmacy, Bucharest and made an Honorary Fellow of The British Pharmacological Society for his contribution to research in to movement disorders.

Peter has worked closely with the pharmaceutical industry for many years and acts as an adviser and consultant to both major pharma and biotech companies. He has a wide knowledge of the drug discovery and drug development process and has been involved from molecule synthesis through to drug registration for use in man. Peter was the Founder, Director and Chief Scientific Officer of Proximagen, a biotech focussed on the treatment and cure of neurodegenerative diseases that was listed on AIMs and subsequently purchased by a US based healthcare company. He is a regular speaker at international meetings and also takes time to speak at Parkinsons disease patient-carer groups across the UK.