Multiple sclerosis (MS) is an autoimmune disease that results in the destruction of the myelin sheath that surrounds nerve fibers of the brain, spinal cord, and optic nerves. As a result, the transmission of nerve impulses becomes impaired, particularly in pathways involved with vision, sensation, and movement. The disease primarily occurs in individuals between the ages of 20 and 40, and women are affected by the disease more often than men. The disease remains enigmatic, with some patients experiencing no symptoms or a remission of the disease in which previously impaired functions such as…mehr
Multiple sclerosis (MS) is an autoimmune disease that results in the destruction of the myelin sheath that surrounds nerve fibers of the brain, spinal cord, and optic nerves. As a result, the transmission of nerve impulses becomes impaired, particularly in pathways involved with vision, sensation, and movement. The disease primarily occurs in individuals between the ages of 20 and 40, and women are affected by the disease more often than men. The disease remains enigmatic, with some patients experiencing no symptoms or a remission of the disease in which previously impaired functions such as vision or motor skills are restored. Other patients experience a course characterized by worsening progress. This book examines the role of neurons in MS and the changes that occur in neurons as a result of MS. It places MS in a new and important perspective that not only explains the basis for symptom production, remission, and progress in MS, but also promises to open up new therapeutic possibilities.Hinweis: Dieser Artikel kann nur an eine deutsche Lieferadresse ausgeliefert werden.
PrefaceContributorsI Structure, Molecular Organization, and Function of Myelinated Axons 1. The Structure of Myelinated Axons in the CNS 2. Dialogues: Communication Between Axons and Myelinating Glia 3. Molecular Specializations at the Glia-Axon Interface 4. Potassium Channel Organization of Myelinated and Demyelinated Axons 5. The Roles of Potassium and Calcium Channels in Physiology and Pathophysiology of AxonsII Neuronal Concomitants of Demyelination 6. The Conduction Properties of Demyelinated and Remyelinated Axons 7. Altered Distributions and Functions of Multiple Sodium Channel Subtypes in Multiple Sclerosis and Its Models 8. Na+ Channel Reorganization in Demyelinated Axons 9. Ion Currents and Axonal Oscillators: A Possible Biophysical Basis for Positive Signs and Symptoms in Multiple Sclerosis 10. Clinical Pharmacology of Abnormal Potassium Channel Organization in Demyelinated AxonsIII Multiple Sclerosis as a Neurodegenerative Disease 11. Pathology of Neurons in Multiple Sclerosis 12. Axonal Degeneration in Multiple Sclerosis: The Histopathological Evidence 13. Natural History of Multiple Sclerosis: When Do Axons Degenerate?IV Measurement of Neuronal Changes in the Clinical Domain 14. Brain Atrophy as a Measure of Neurodegeneration and Neuroprotection 15. MRI-Clinical Correlations in Multiple Sclerosis: Implications for Our Understanding of Neuronal Changes 16. Electrophysiological Correlates of Relapse, Remission, Persistent Sensorimotor Deficit, and Long-Term Recovery Processes in Multiple SclerosisV Cellular and Molecular Mechanisms of Axonal Degeneration in Multiple Sclerosis 17. Inflammation and Axon Degeneration 18. Nitric Oxide and Axonal Pathophysiology 19. Molecular Mechanisms of Calcium Influx in Axonal Degeneration 20. Axonal Damage and Neuron Death in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis: The Role of Calpain 21. Mutations of Myelination-Associated Genes That Affect Axonal IntegrityVI Other Aspects of Neuronal Injury in Multiple Sclerosis 22. Neuronal Blocking Factors in Demyelinating Diseases 23. Evidence for Neuronal Apoptosis in Demyelinating CNS DiseasesVII Lessons from the Peripheral Nervous System 24. Mechanisms Underlying Wallerian Degeneration 25. AMAN: What It Teaches Us about Mechanisms Underlying Axonal Injury VIII Prognosis, Reparative Mechanisms, and Therapeutic Approaches 26. Axonal Degeneration as a Predictor of Outcome in Neurological Disorders 27. Remyelination as Neuroprotection 28. Transplantation of Peripheral-Myelin-Forming Cells to Repair Demyelinated Axons 29. Blocking the Axonal Injury Cascade: Neuroprotection in Multiple Sclerosis and Its Models 30. Functional Brain Reorganization and Recovery after Injury to White MatterIndex
PrefaceContributorsI Structure, Molecular Organization, and Function of Myelinated Axons 1. The Structure of Myelinated Axons in the CNS 2. Dialogues: Communication Between Axons and Myelinating Glia 3. Molecular Specializations at the Glia-Axon Interface 4. Potassium Channel Organization of Myelinated and Demyelinated Axons 5. The Roles of Potassium and Calcium Channels in Physiology and Pathophysiology of AxonsII Neuronal Concomitants of Demyelination 6. The Conduction Properties of Demyelinated and Remyelinated Axons 7. Altered Distributions and Functions of Multiple Sodium Channel Subtypes in Multiple Sclerosis and Its Models 8. Na+ Channel Reorganization in Demyelinated Axons 9. Ion Currents and Axonal Oscillators: A Possible Biophysical Basis for Positive Signs and Symptoms in Multiple Sclerosis 10. Clinical Pharmacology of Abnormal Potassium Channel Organization in Demyelinated AxonsIII Multiple Sclerosis as a Neurodegenerative Disease 11. Pathology of Neurons in Multiple Sclerosis 12. Axonal Degeneration in Multiple Sclerosis: The Histopathological Evidence 13. Natural History of Multiple Sclerosis: When Do Axons Degenerate?IV Measurement of Neuronal Changes in the Clinical Domain 14. Brain Atrophy as a Measure of Neurodegeneration and Neuroprotection 15. MRI-Clinical Correlations in Multiple Sclerosis: Implications for Our Understanding of Neuronal Changes 16. Electrophysiological Correlates of Relapse, Remission, Persistent Sensorimotor Deficit, and Long-Term Recovery Processes in Multiple SclerosisV Cellular and Molecular Mechanisms of Axonal Degeneration in Multiple Sclerosis 17. Inflammation and Axon Degeneration 18. Nitric Oxide and Axonal Pathophysiology 19. Molecular Mechanisms of Calcium Influx in Axonal Degeneration 20. Axonal Damage and Neuron Death in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis: The Role of Calpain 21. Mutations of Myelination-Associated Genes That Affect Axonal IntegrityVI Other Aspects of Neuronal Injury in Multiple Sclerosis 22. Neuronal Blocking Factors in Demyelinating Diseases 23. Evidence for Neuronal Apoptosis in Demyelinating CNS DiseasesVII Lessons from the Peripheral Nervous System 24. Mechanisms Underlying Wallerian Degeneration 25. AMAN: What It Teaches Us about Mechanisms Underlying Axonal Injury VIII Prognosis, Reparative Mechanisms, and Therapeutic Approaches 26. Axonal Degeneration as a Predictor of Outcome in Neurological Disorders 27. Remyelination as Neuroprotection 28. Transplantation of Peripheral-Myelin-Forming Cells to Repair Demyelinated Axons 29. Blocking the Axonal Injury Cascade: Neuroprotection in Multiple Sclerosis and Its Models 30. Functional Brain Reorganization and Recovery after Injury to White MatterIndex
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