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  • 1
    Online Resource
    Online Resource
    Newark :John Wiley & Sons, Incorporated,
    Keywords: Hormones. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (405 pages)
    Edition: 2nd ed.
    ISBN: 9783527633845
    DDC: 612.8
    Language: English
    Note: Intro -- Hormones in Neurodegeneration, Neuroprotection, and Neurogenesis -- Contents -- List of Contributors -- Part I Estrogens, Progestins, Allopregnanolone and Neuroprotection -- 1 Interactions of Estradiol and Insulin-like Growth Factor-I in Neuroprotection: Implications for Brain Aging and Neurodegeneration -- 1.1 Introduction: Hormones, Brain Aging, and Neurodegeneration -- 1.2 Estradiol, IGF-I, Brain Aging, and Neuroprotection -- 1.3 Molecular Interactions of Estrogen Receptors and IGF-I Receptor in the Brain -- 1.4 Regulation of IGF-I Receptor Signaling by Estradiol in the Brain -- 1.5 Regulation of Estrogen Receptor Transcriptional Activity by IGF-I in Neural Cells -- 1.6 Implications of the Cross Talk between Estrogen Receptors and IGF-I Receptors for Brain Aging, and Neurodegeneration -- Acknowledgment -- References -- 2 Structure-Nongenomic Neuroprotection Relationship of Estrogens and Estrogen-Derived Compounds -- 2.1 Introduction -- 2.2 In vitro Assessments of Structure-Neuroprotective Activity Relationships -- 2.2.1 Estradiol and Other Known Estratrienes -- 2.2.2 A-Ring Derivatives -- 2.2.3 B- and C-Ring Derivatives -- 2.2.4 D-Ring Derivatives -- 2.2.5 Correlation between Inhibition of TBARs and Protection against Glutamate and IAA -- 2.2.6 Estrogen Receptor Binding -- 2.2.7 Correlation between Inhibition of TBARs or Neuroprotection and ER Binding -- 2.2.8 Interpretation of In vitro Findings -- 2.3 In vivo Assessment of Structure-Neuroprotective Activity Relationships -- 2.4 In vitro Assessment of Structure-Cell Signaling Relationships -- 2.5 Summary -- Acknowledgment -- References -- 3 Progestins and Neuroprotection: Why the Choice of Progestin Matters -- 3.1 Introduction -- 3.2 The Biology of Progesterone -- 3.3 Membrane-Associated Progesterone Receptors -- 3.4 Progesterone-Induced Protection. , 3.5 Mechanisms Underlying Progesterone's Protective Effects -- 3.6 Medroxyprogesterone Acetate -- Acknowledgments -- References -- 4 Endogenous and Synthetic Neurosteroids in the Treatment of Niemann-Pick Type C Disease -- 4.1 Introduction -- 4.2 Niemann-Pick Type C Disease as a Model of Disrupted Neurosteroidogenesis -- 4.3 Steroidogenesis and Neurosteroidogenesis in NP-C -- 4.4 Treatment of NP-C Mice with Allopregnanolone -- 4.5 Mechanism of Allopregnanolone Action: GABAA Receptor -- 4.6 Mechanism of Allopregnanolone Action: Pregnane-X Receptor -- 4.7 Mechanism of Allopregnanolone Action: Reduction of Cellular Oxidative Stress -- 4.8 Conclusions - Mechanisms of Allopregnanolone Action in Treatment of NP-C and Other Neurodegenerative Diseases -- Acknowledgments -- References -- Part II Glucocorticoids, Dehydroepiandrosterone, Neuroprotection and Neuropathy -- 5 Glucocorticoids, Developmental ''Programming,'' and the Risk of Affective Dysfunction -- 5.1 Introduction to Programming -- 5.2 Programming -- 5.2.1 Epidemiology -- 5.2.2 Birth Weight and Neuropsychiatric Disorders -- 5.3 Glucocorticoids and Fetal Development -- 5.4 Glucocorticoids: the Endocrine Programming Factor -- 5.4.1 Placental 11β-HSD2: a Barrier to Maternal Glucocorticoids -- 5.4.2 Glucocorticoid Programming -- 5.4.3 Transgenerational Effects -- 5.4.4 The Placenta -- 5.4.5 A Common Mechanism? -- 5.5 Fetal Tissue Glucocorticoid Sensitivity -- 5.6 Stress and Glucocorticoids: Key Programmers of the Brain -- 5.6.1 Programming the HPA Axis -- 5.6.2 Sex-Specific Effects -- 5.6.3 Programming Behavior -- 5.7 CNS Programming Mechanisms -- 5.7.1 The GR Gene: a Common Programming Target? -- 5.7.2 Epigenetics -- 5.8 Glucocorticoid Programming in Humans -- 5.8.1 Clinical Use of Prenatal Glucocorticoid Therapy -- 5.8.2 Consequences of Human Fetal Glucocorticoid Overexposure. , 5.8.3 Programming and Posttraumatic Stress Disorder (PTSD) -- 5.8.4 Programming Other Glucocorticoid Metabolizing Enzymes -- 5.9 Future Perspectives and Therapeutic Opportunities -- 5.10 Overview -- References -- 6 Regulation of Structural Plasticity and Neurogenesis during Stress and Diabetes -- Protective Effects of Glucocorticoid Receptor Antagonists -- 6.1 The Stress Response -- 6.2 HPA Axis and Glucocorticoids -- 6.3 Glucocorticoid Actions -- 6.4 Feedback Regulation -- 6.5 Stress and Depression -- 6.6 Stress-Induced Viability Changes in the Hippocampus: Effect on Function, Volume, Cell Number, and Apoptosis -- 6.7 Effects of Stress on Dendritic Atrophy, Spine, and Synaptic Changes -- 6.8 Adult Hippocampal Neurogenesis -- 6.9 Effect of Stress on Adult Hippocampal Neurogenesis -- 6.10 Normalization of the Effects of Stress on the Hippocampus by Means of GR Blockade -- 6.11 Normalization of Hippocampal Alterations during Diabetes Mellitus Using the GR Antagonist Mifepristone -- 6.12 Concluding Remarks -- Acknowledgments -- Disclosure -- References -- 7 Neuroactive Steroids and Peripheral Neuropathy -- 7.1 Introduction -- 7.2 Regulation of Neuroactive Steroid Responsiveness in Peripheral Nerves -- 7.2.1 Synthesis and Metabolism of Neuroactive Steroids -- 7.2.2 Classical and Nonclassical Steroid Receptors are Expressed in Peripheral Nerves -- 7.3 Schwann Cell Responses to Neuroactive Steroids -- 7.4 Sexually Dimorphic Changes of Neuroactive Steroid Levels Induced by Pathology in Peripheral Nerves -- 7.5 Neuroactive Steroids as Protective Agents in PNS -- 7.5.1 Aging Process -- 7.5.2 Physical Injury -- 7.5.3 Diabetic Neuropathy -- 7.6 Chemotherapy-Induced Peripheral Neuropathy -- 7.7 Concluding Remarks -- Acknowledgments -- References -- 8 Neuroprotective and Neurogenic Properties of Dehydroepiandrosterone and its Synthetic Analogs -- 8.1 Introduction. , 8.2 Neuroprotective and Neurogenic Effects of DHEA in Hippocampal Neurons -- 8.3 Neuroprotective Effects of DHEA in Nigrostriatal Dopaminergic Neurons -- 8.4 Neuroprotective Effects of DHEA in Autoimmune Neurodegenerative Processes -- 8.5 Neuroprotective Effects of DHEA against Brain Ischemia and Trauma -- 8.6 Signaling Pathways Involved in the Effects of DHEA on Neuronal Cell Fate -- 8.7 Therapeutic Perspectives of DHEA and its Synthetic Analogs in Neurodegenerative Diseases -- References -- 9 Neurosteroids and Pain Christine Patte-Mensah, Laurence Meyer, V´eronique Schaeffer, Cherkaouia -- 9.1 Introduction -- 9.2 General Background on Neurosteroids -- 9.3 Overview on Pain -- 9.4 Involvement of Endogenous Neurosteroids in the Control of Pain -- 9.4.1 Evidence for the Local Production of Neurosteroids in the Spinal Circuit -- 9.4.2 Endogenous Neurosteroids and Pain Modulation -- 9.5 Conclusion -- Acknowledgments -- References -- Part III Polypeptide Hormones and Neuroprotection -- 10 The Insulin/IGF-1 System in Neurodegeneration and Neurovascular Disease -- 10.1 Introduction -- 10.2 Insulin and Insulin Growth Factors -- 10.3 Local versus Systemic Actions -- 10.4 Insulin/IGF Signaling Pathway -- 10.5 The Insulin/IGF Axis in the Brain -- 10.6 Insulin/IGF and Neuroprotection -- 10.7 Alzheimer's Disease -- 10.8 Parkinson's Disease -- 10.9 Vascular Dementia -- 10.10 Neurovascular Degeneration -- 10.11 Conclusion -- References -- 11 Leptin Neuroprotection in the Central Nervous System -- 11.1 Introduction -- 11.1.1 Origin, Source, and Structure of Leptin -- 11.1.2 Functions of Leptin -- 11.1.3 Leptin Receptors -- 11.1.4 Leptin Transport across the Blood-Brain Barrier -- 11.2 Mutation of Leptin or Leptin Receptors -- 11.3 Neurotrophic Role of Leptin -- 11.4 Leptin Neuroprotection against Disorders of the Central Nervous System. , 11.4.1 Acute Neurological Disorders -- 11.4.2 Neurodegenerative Diseases and Other Disorders -- 11.4.3 Leptin Neuroprotective Mechanisms -- 11.5 Significance -- References -- 12 Somatostatin and Neuroprotection in Retina -- 12.1 Introduction -- 12.2 Somatostatin and Related Peptides -- 12.3 Somatostatin Receptors and Signaling -- 12.4 Somatostatin and its Receptors in Retina -- 12.5 Localization of Somatostatin Receptors in Retinal Neurons -- 12.5.1 Sst1 -- 12.5.2 Sst2 -- 12.5.3 Sst3 -- 12.5.4 Sst4 -- 12.5.5 Sst5 -- 12.6 Somatostatin Receptor Function in Retinal Circuitry -- 12.6.1 Effects on Glutamate Release -- 12.6.2 Effects on Dopamine Release -- 12.6.3 Effects on Nitric Oxide/GMP -- 12.6.4 Effects on Somatostatin Release -- 12.7 Neuroprotection by Somatostatin Analogs -- 12.7.1 Retinal Ischemia and Excitotoxicity -- 12.7.2 Anti-Ischemic Actions of SRIF -- 12.7.2.1 Ex vivo Studies -- 12.7.2.2 In vivo Studies -- 12.8 Mechanisms of SRIF's Neuroprotection -- 12.8.1 Involvement of NO/cGMP -- 12.8.2 NO/cGMP Mediates SRIF's Neuroprotective Effects -- 12.9 Therapeutic Potential of Somatostatin Agents -- 12.10 Conclusions -- Acknowledgments -- Abbreviations -- References -- 13 Neurotrophic Effects of PACAP in the Cerebellar Cortex -- 13.1 Expression of PACAP and its Receptors in the Developing Cerebellum -- 13.2 Effects of PACAP on Granule Cell Proliferation -- 13.3 Effects of PACAP on Granule Cell Migration -- 13.4 Effects of PACAP on Granule Cell Survival -- 13.5 Effects of PACAP on Granule Cell Differentiation -- 13.6 Functional Relevance -- Acknowledgments -- References -- 14 The Corticotropin-Releasing Hormone in Neuroprotection -- 14.1 Introduction -- 14.2 The CRH Family of Proteins and Molecular Signal Transduction -- 14.3 From the Physiology to the Pathophysiology of CRH -- 14.4 CRH and Neurodegenerative Conditions. , 14.5 Protective Activities of CRH.
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 458 (1985), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2323
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. There are several theories about the physiologic regeneration of adrenals and maintenance of physiologic steroid secretion after subtotal loss of adrenal cortical cells. According to the cell migration theory, adrenocytes from the zona glomerulosa migrate centripetally toward the medulla. This theory is opposed by the zonal theory according to which each zone resplenishes its cells independently. What these theories have in common is that they are based on data from the intact adrenal gland. We transplanted purified glomerulosa cells under the kidney’s capsule of Lewis rats. The tissue was removed 30, 60, 90, and 150 days after transplantation to investigate the presence of two specific enzymes that are responsible for the secretion of aldosterone and corticosterone. Cytochrome p-450as is specific for glomerulosa cells producing aldosterone, and cytochrome p-45011β is specific for fasciculata cells producing corticosterone. After sequencing the genetic code of these enzymes it became possible to demonstrate expression of the enzymes by in situ hybridization. The transplanted glomerulosa cells turned their enzymatic property to fasciculata cells expressing cytochrome p-45011β. Our results suggest that glomerulosa cells are able to take over the physiologic function of a whole adrenal cortex in the absence of fasciculata cells, and that they are sufficient to maintain the function of the adrenal cortex.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature medicine 10 (2004), S. 704-711 
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Niemann–Pick type C (NP-C) disease is a fatal, autosomal recessive, childhood neurodegenerative disease. The NP-C mouse recapitulates the cholesterol and sphingolipid storage, onset of neurological deficits, histopathological lesions, Purkinje cell loss and early death typical of the most ...
    Type of Medium: Electronic Resource
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