The Strict Concept of Specificity as Multiple Sclerosis Pathogenesis

Preface; The Adaxonal Myelin Layer Triggers and Destabilizes Multiple Sclerosis Pathogenesis; Pathogenic Systems of Heterogeneity in Distinct Onset versus Progression Phases of Multiple Sclerosis in Terms of Amplifying Overlap of Immune Reactivities; Variability of Expressivity in Multiple Sclerosis Involves Pathogenic Diversity in Lesion Progression and in Attempted Lesion Reconstitution; Tightly Coupled Demyelination and Remyelination Constitute Basic Biology of Persistence in the Multiple Sclerosis Plaque in Terms of Neuronal/axonal Primal Injury Progression; The Essential Links between Genetic Susceptibility and Environmental Pathogens in Multiple Sclerosis Progression and Initiation; Performance Reactivation of Immune Response Defines Multiple Sclerosis Progression as Systems of Overlap Spread and Amplification via Endothelial Cells; A Multi-Factorial Genesis of the Multiple Sclerosis Triggering Event and of the Propagation of Progressing Lesions in the Central Nervous System; Attributes of Patterned Injury in Multiple Sclerosis Sequential Plaque Definitionthe Primal Vascular Wall Paradigm; Integral Biologic System-Induced Energy Failure Allows and Further Establishes Neurodegeneration and Inflammatory Demyelination in Multiple Sclerosis; Constitutive and Acquired Formulas of Transformation in Multiple Sclerosis; The Outcome of the Individual Multiple Sclerosis Plaque as Pre-Determined Parameter in Disease Progression or Potential Recovery; Elemental Context Definition in Integral Geography of Multiple Sclerosis Lesions; An Integral Formulation of Targeting Combinations of the Innate and Adaptive Immune Systems in Ms in Terms of Activated Vasculitis; Dimensions of Co-Operative Overlap of a Primal Autoimmunity of Contactual Repeated Antigenic Characterization in Multiple Sclerosis; Autoimmunity as Specific Enhanced Response to Cell Injury in Multiple Sclerosis Persistence and Re-Modulation in Terms of the Gut Microbiota Reconstitutive Profiles; Systems of Integrity as Interacting and Individual Subsystems in Multiple Sclerosis Networks in Terms of Cns Impaired Immune Privileged Status in Neuroinflammation; Instability of the Inflammasome Induces Eventual Autoimmunity in Multiple Sclerosis; Diversity in Injury Pathways Incorporated as Unitary Targeting Events in Multiple Sclerosis; An Essential Permissive Microenvironment as Primarily Passive Accumulation of Multiple Sclerosis Lesion Byproducts Redefines Disease Pathogenesis; Proposed Dynamics of Predetermination of Multiple Sclerosis Injury in Terms of Concurrent Potentiality for Recovery; Interface Interactivities as Systemic Biology Reconstitution in Multiple Sclerosis; Profiles of Transforming Activations of Immune Cells as Infiltrative Dimensions in Definition of T Cd4+ Helper Cells in Neuroinflammation of Multiple Sclerosis Type; Index.