Comparative Neuropathology of Chronic Experimental Allergic Encephalomyelitis and Multiple Sclerosis
General Material Designation
[Book]
First Statement of Responsibility
Hans Lassmann
EDITION STATEMENT
Edition Statement
Softcover reprint of the original 1st ed. 1983
.PUBLICATION, DISTRIBUTION, ETC
Name of Publisher, Distributor, etc.
Berlin Springer Berlin
Date of Publication, Distribution, etc.
2014
PHYSICAL DESCRIPTION
Specific Material Designation and Extent of Item
IX, 138 Seiten in 1 Teil 34 schw.-w. Illustrationen 244 x 170 mm
SERIES
Series Title
Schriftenreihe Neurologie / Neurology Series, 25
CONTENTS NOTE
Text of Note
1 Introduction.- 2 The Spectram of Inflammatory Demyelinating Diseases.- 2.1 Experimental Models.- 2.2 Human Diseases.- 3 Allergic Encephalomyelitis in Humans.- 4 The Pathology of Inflammatory Demyelinating Lesions.- 4.1 Inflammatory Reaction.- 4.1.1 Inflammation in Experimental Allergic Encephalomyelitis.- 4.1.2 The Inflammatory Response in Human Inflammatory Demyelinating Diseases.- 4.2 Vascular Pathology.- 4.2.1 Vascular Pathology in EAE.- 4.2.2 Vascular Pathology in Multiple Sclerosis.- 4.3 Blood-Brain Barrier.- 4.3.1 Blood-Brain Barrier and Blood-CSF Barrier Leakage Under Physiological Conditions.- 4.3.2 The Diffusion of Proteins in the Extracellular Space of the Brain.- 4.3.3 Mechanisms and Structural Correlates of Blood- Brain Barrier Damage.- 4.3.4 The Blood-Brain Barrier in Experimental Allergic Encephalomyelitis.- 4.3.5 Implications of Blood-Brain Barrier Permeability on the Distribution of EAE Lesions Within the CNS.- 4.3.6 The Blood-Brain Barrier in Multiple Sclerosis.- 4.4 Demyelination and Myelin Degradation.- 4.4.1 Initial Stages of Demyelination in EAE.- 4.4.2 Myelin Degradation and Removal of Debris in EAE.- 4.4.3 Demyelination and Myelin Degradation in Multiple Sclerosis.- 4.5 The Fate of Oligodendroglia.- 4.5.1 Oligodendrocytes in EAE Lesions.- 4.5.2 Oligodendroglia in Multiple Sclerosis.- 4.6 Remyelination.- 4.6.1 Remyelination in Acute and Chronic EAE.- 4.6.2 Remyelination in Multiple Sclerosis.- 4.7 Sclerosis.- 4.7.1 Astroglial Reaction in the Lesions of Acute and Chronic EAE.- 4.7.2 Gliosis in Multiple Sclerosis.- 4.8 Axonal and Neuronal Pathology.- 4.8.1 Experimental Allergic Encephalomyelitis.- 4.8.2 Multiple Sclerosis.- 4.9 Meningeal Pathology.- 4.9.1 Experimental Allergic Encephalomyelitis.- 4.9.2 Multiple Sclerosis.- 4.10 Peripheral Nervous System Pathology.- 4.10.1 PNS Involvement in Different Models of Chronic EAE.- 4.10.2 Peripheral Nervous System Involvement in Multiple Sclerosis.- 4.11 Patterns of Plaque Growth.- 4.11.1 Plaque Growth in Chronic EAE.- 4.11.2 Mechanisms of Plaque Growth in Multiple Sclerosis.- 4.12 Lesional Topography in the CNS.- 4.12.1 Lesional Distribution in EAE.- 4.12.2 Lesional Topography in Human Inflammatory Demyelinating Diseases.- 4.13 The Variability of Inflammatory Demyelinating Lesions.- 4.14 EAE as a Model of Human Inflammatory Demyelinating Diseases.- 5 Immunopathogenetic Considerations.- 5.1 Transfer Studies.- 5.2 The Possible Role of Autoantigens in the Pathogenesis of Inflammatory Demyelinating Lesions.- 5.3 Conclusions.- 5.3.1 The Variability of EAE Lesions as an Expression of Multiple Antigens and Effector Mechanisms.- 5.3.2 The Compartmentalization of the Immune Reaction and Its Consequences for the Study of Chronic EAE Pathogenesis.- 5.3.3 Implications for Future Research in Human Inflammatory Demyelinating Diseases.- 6 Addendum: Material and Methods - Models of Chronic EAE.- 6.1 Material and Methods.- 6.1.1 Animal Care.- 6.1.2 Clinical Grading.- 6.1.3 Sensitization Procedure.- 6.1.4 Sampling of Animals.- 6.1.5 Human Material.- 6.2 Factors Modifying the Development of Chronic EAE Models.- 6.2.1 Guinea Pig Strains.- 6.2.2 Antigen Dose.- 6.2.3 Age of the Animals at the Time of Sensitization.- 6.2.4 Inoculation Site.- 6.2.5 Amount of Mycobacterium in the Adjuvant.- 6.2.6 Spinal Cord Subfractions.- 6.2.7 Chronic EAE in Sprague Dawley Rats.- 6.2.8 Conclusions.- 7 References.