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의학서적전문 "성보의학서적"의 신간의학도서입니다.

The emerging understanding of age-related neurological disorders suggeststhat notions of a single causal gene/toxin being responsible is likely incorrect. Neurological disorders likely arise due to a unique intersection of multiple genetic and toxic factors combined with additional contributions of age, stage of development, immune system actions, and more. This perspective leads to the view that rather than reflecting only one pathway to end state disease, each is a spectrum disorder and each individual case is therefore unique.

Neural Dynamics of Neurological Disease argues for a fundamental rethinking of what we think we know about neurological disorders, how these arise and progress and, crucially, what might be done to “cure” them. Chapters first introduce the concept of neural dynamics of neurological disease, then examine various diseases and give examples of the interplay of elements such as neural systems, cell types, and biochemical pathways which can contribute to disease. Concluding chapters point the way forward to how the emerging notion of neurological disease as a dynamic process may lead to more successful treatment options.

Providing a cross disciplinary approach to understanding the origin and progression of neurological disease, Neural Dynamics of Neurological Disease is a timely and valuable resource for neuroscientists, researchers and clinicians.

-도서목차-

List of Figures

List of Tables

Preface

Acknowledgments

Part I The Dynamics of Neurological Disease

1 The Dynamics of Neurological Disease: Current Views and Key Issues

1.1 From the Preface

1.2 The Complexity of Human Neurological Diseases

1.3 The Nervous System as an Archetypical Complex System

1.4 CNS Signaling Failures: Implications for Neurological Disease

1.5 History and Key Characteristics of the Age-Dependent Neurological Diseases

1.6 The Fractal Nature of Complexity in the CNS

2 Clinical and Economic Features of Age-Related Neurological Diseases

2.1 From the Preface

2.2 Parkinson’s Disease

2.2.1 Neuropathological Features

2.2.2 The Parkinsonisms

2.2.3 Rating Schemes

2.2.3.1 Hoehn and Yahr Scale

2.2.3.2 Modified Hoehn and Yahr Scale

2.2.3.3 Schwab and England Activities of Daily Living Scale

2.2.3.4 Unified Parkinson’s Disease Rating Scale

2.2.4 Progression

2.2.5 Other Organ System Involvement

2.2.6 Parkinson’s Disease Clusters

2.2.7 Risk Factors

2.2.8 Current Treatment Options

2.2.9 Animal Models

2.2.10 Parkinson’s Disease in Relation to Other Neurological Diseases

2.2.11 Demographics

2.2.12 Incidence and Prevalence

2.2.12.1 United States and Canada

2.2.12.2 Worldwide

2.2.13 Changes in Incidence/Prevalence over the Last 30 Years

2.2.13.1 United States and Canada

2.2.14 Costs

2.2.14.1 Cost Per Patient

2.2.14.2 Societal Costs

2.2.14.3 Projected Cost Increases

2.3 Amyotrophic Lateral Sclerosis

2.3.1 Loci of Onset

2.3.2 Neuropathological Features

2.3.3 Rating Schemes

2.3.3.1 El Escorial Diagnostic Criteria

2.3.3.2 ALS Functional Rating Scale

2.3.3.3 Forced Vital Capacity

2.3.4 Progression

2.3.5 Rates of Disease Progression

2.3.6 Age of Onset and Sex Distribution

2.3.7 Other Organ System Involvement

2.3.8 ALS Clusters

2.3.9 Risk Factors

2.3.10 Current Treatment Options

2.3.11 ALS in Relation to Other Neurological Diseases and Disorders: Cognitive Impairment

2.3.12 ALS and Other CNS Regions

2.3.13 Animal Models

2.3.14 Incidence and Prevalence

2.3.14.1 United States and Canada

2.3.15 Changes in Incidence/Prevalence over the Last 30 Years

2.3.15.1 United States

2.3.15.2 Canada

2.3.15.3 Worldwide

2.3.16 Costs

2.3.16.1 Cost Per Patient

2.3.16.2 Societal Costs

2.4 Alzheimer’s Disease

2.4.1 Neuropathological Features

2.4.2 Rating Schemes

2.4.2.1 Global Deterioration Scale

2.4.2.2 Functional Assessment Staging

2.4.2.3 Clinical Dementia Rating

2.4.3 Other Organ System Involvement

2.4.4 Alzheimer’s Disease Clusters

2.4.5 Risk Factors

2.4.6 Current Treatment Options

2.4.7 Demographics

2.4.8 Incidence and Prevalence

2.4.8.1 United States

2.4.8.2 Canada

2.4.9 Changes in Incidence/Prevalence over the Last 30 Years

2.4.9.1 United States

2.4.10 Costs

2.4.10.1 Costs Per Patient

2.4.10.2 Societal Costs

2.4.10.3 Projected Cost Increases

2.5 Summary of the Data on the Progressive, Age-Related Neurological Diseases

2.6 Neural Loci and Mechanisms of Action

3 Spectrum of Neurological Disease, Clusters, and Ubiquity

3.1 From the Preface

3.2 Spectrums of Neurological Disease

3.3 The Dimension of the Problem when Assessing Potential Causal Factors in Neurological Diseases

3.4 Neurological Disease Clusters

3.4.1 Lathyrism

3.4.2 Minimata

3.4.3 Domoic Acid

3.4.4 Summary

3.5 Ubiquity

3.6 Nested Complex Systems: Proximal versus Distal Events as They May Relate to Neurological Diseases

3.7 The Path to “Curing” Neurological Diseases

4 Complexity, Cascading Failures, and Neurological Diseases

4.1 From the Preface

4.2 Introduction to Complexity Theory and Complex Systems

4.3 Computer Programs and Computer Crashes

4.4 Biosemiosis in the CNS (Part 1)

4.4.1 Degraded Biological Signals in CNS Pathology

4.5 Complexity in the CNS and the Impact of Genetic and Environmental Insults

4.6 Tipping Points and Time Lines of Disease Progression

5 Genetic Determinants of Neurological Disease

5.1 From the Preface

5.2 Causality versus Coincidence

5.3 Actions of Mutant Genes in Neurological Disease

5.3.1 Huntington’s Disease

5.4 Genetic Mutations Linked to Parkinson’s Disease

5.4.1 α-synuclein

5.4.2 LRRK2

5.4.3 Lesser Genes Associated with Autosomal-Recessive Forms of Parkinson’s Disease

5.4.4 Summary

5.5 Genetic Mutations Linked to ALS

5.5.1 SOD1

5.5.2 TARDBP

5.5.3 FUS

5.5.4 UBQLN2

5.5.5 C9orf72

5.5.6 Summary

5.6 Genetic Mutations Linked to Alzheimer’s Disease

5.6.1 APP

5.6.2 Presenilin 1 (PSEN1)

5.6.3 Presenilin 2 (PSEN2)

5.7 Genes and Neurological Disease: Some General Considerations

6 Environmental Determinants of Neurological Disease and Gene–Toxin Interactions

6.1 From the Preface

6.2 Toxins and Neurological Diseases

6.2.1 Pesticides, etc.

6.2.2 Toxic Metals

6.2.3 Amino Acids, Natural and Human-Made

6.2.4 Steryl Glucosides

6.2.5 Bisphenols

6.2.6 Summary

6.3 Aluminum and Neurological Disease

6.3.1 Some Background to Aluminum Chemistry and the Intersection of Aluminum with the Biosphere

6.4 Single- vs. Multiple-Hit Models of Neurological Disease: Gene–Toxin Interactions

6.5 Genetic Susceptibility Factors

6.5.1 Toxin-Triggering Genetic Alterations and Gene Expression Levels

6.5.2 miRNA Alterations in Gene Expression

6.6 Biosemiosis (Part 2)

6.6.1 Aluminum and Failed Biosemiosis

6.7 Gene–Toxin Interactions and Cascading Failures

6.8 Genes and Toxins in Neurological Disease: Penultimate Thoughts

6.9 And, Finally, the Microbiome

7 The Mystery and Lessons of ALS-PDC

7.1 From the Preface

7.2 Neurological Disease Clusters and ALS-PDC

7.3 History and Features of ALS-PDC

7.4 Cycad and ALS-PDC

7.4.1 Human Consumption of Cycad

7.4.2 Cycad’s Links to ALS-PDC

7.5 Amino Acid Toxins in Cycad and ALS-PDC

7.6 Non-Amino Acid Toxins Linked to ALS-PDC

7.7 Aluminum and Ionic Etiologies for ALS-PDC

7.8 Still Other Molecules Causal to ALS-PDC

7.9 What is the Current View on the Importance of ALS-PDC?

7.10 Complexity of Neurological Diseases as Viewed from Guam

Part II Age and Time Lines of Neurological Disease

8 Neurological Disease Models and their Discontents: Validity, Replicability, and the Decline Effect

8.1 From the Preface

8.2 Modeling Human Neurological Diseases: Possibilities and Pitfalls

8.3 Considerations Regarding Model Systems

8.4 Model Systems and their Discontents

8.4.1 Age and Time in In Vivo Models as a Function of Species

8.4.2 Replicability and the Problems Created by the Absence of the Same

8.4.3 The “Decline Effect”

8.5 Is There an Ideal Model for Studying Neurological Diseases? General Considerations

8.6 Specific Considerations for Ideal Model-System Approaches in ALS

8.6.1 ALS Considered from the Perspective of Model Systems: Lost in Translation

8.7 Alternative Views of Neurological Disease and Model-Systems Approaches: Multiple-Hit Etiologies

9 The Progression and the Time Line of Neurological Disease

9.1 From the Preface

9.2 Creating Disease Time Lines: The Framingham Study

9.3 Time Lines of Neurological Disease

9.3.1 Braak Staging for Parkinson’s Disease

9.3.2 Braak Staging for Alzheimer’s Disease

9.3.3 Problems in Post-Clinical Staging

9.3.4 Staging of Clinical Features and Pathology

9.4 Back to a Multiple-Hit Disease Consideration

9.5 Haecceity and Quiddity in Context to Biosemiosis and Multiple Hits

9.6 Some Final Thoughts on Time Lines of Neurological Disease: Differentiation and Neurogenesis

10 Development, Aging, and Neurological Disease

10.1 From the Preface

10.2 The Fetal Basis of Adult Disease Hypothesis

10.3 ASD as a Developmental Neurological Disorder

10.3.1 Etiology of ASD

10.3.2 Juvenile Schizophrenia

10.3.3 Juvenile-Onset Forms of ALS and Other Neurological Disorders

10.4 Toxins and Developmental CNS Disorders

10.5 Developmental versus Mature CNS Disorders

Part III Interactions and Synergies in Neurological Disease

11 CNS–Immune System Interactions and Autoimmunity

11.1 From the Preface

11.2 Immunity and the CNS, an Introduction to a Complex Topic

11.2.1 Innate versus Adaptive Immune Systems and their Roles in CNS Development

11.2.2 The Role of Microglia in Neurological Diseases

11.3 CNS–Immune System Interactions: More Detailed Considerations

11.3.1 Pathogen and Aluminum Activation of the Immune System in Relation to the CNS

11.3.2 HPA–Immune System Interactions

11.4 Autoimmunity

11.4.1 Bidirectional Role of Immune System–CNS Interactions and Autoimmunity during Neuronal Development

11.4.2 Autoimmunity and Neurological Diseases

11.4.3 The Age-Related, Progressive Neurological Diseases and Autoimmunity

11.5 Immune System Signaling Errors and Autoimmunity in ASD and Other Neurological Disorders

11.5.1 Aluminum’s Role in Immune-System Signaling Errors

11.6 Laterality and Autoimmunity in Neurological Diseases

11.7 Other System Disorders in Neurological Diseases: More Evidence for Autoimmunity?

11.8 Are There Infectious Disease Links to Neurological Diseases?

12 The Impact of Synergy of Factors in Neurological Disease

12.1 From the Preface

12.2 Synergistic and Additive Effects in General and as Applied to CNS Diseases

12.3 Gene–Environment (Toxin) Interactions in Non-neuronal Systems

12.3.1 Genetic Polymorphism and Alcoholism

12.3.2 Genetic Polymorphism and Lactose Intolerance

12.3.3 Genetic Polymorphism and Gluten Intolerance

12.4 Gene–Environment (Toxin) Interactions in Neurological Disease

12.4.1 Summary of Gene–Toxin Interactions in Relation to Neurological Disease

12.5 Levels of Complexity in Gene–Toxin Interactions: Implications for Current and Future Therapeutics

Part IV Transition and Politics in Neurological Disease

13 The Current Status of Neurological Disease Treatments

13.1 From the Preface

13.2 Current Therapeutic Approaches to Treating Neurological Diseases

13.2.1 Drug Therapies

13.2.2 Other Proposed Therapies for Alzheimer’s Disease

13.2.3 Surgical Interventions

13.2.4 Prospects for Neurogenesis as a Treatment for Neurological Disease

13.2.5 Gene Therapy

13.3 Summary

14 The Future of Translational Research in Neurological Disease

14.1 From the Preface

14.2 Comparing Traumatic Brain Injury to Neurological Diseases

14.3 ALS and Polio: Comparing the Nature of Neural Degeneration and Progression in the Two Diseases

14.4 Neurological Diseases as Spectrum Disorders: Implications for Therapy

14.4.1 Parkinson’s and Alzheimer’s Diseases

14.4.2 Progranulin as a Potential Therapeutic in Neurological Diseases

14.5 Cystic Fibrosis and Gene Therapy

14.6 Restoring CNS Function: What Is the Bottom Line?

14.7 Biosemiosis (Part 3) and True Narrative Representations

15 Defining the Limits for Neurological Disease Treatments

15.1 From the Preface

15.2 The Complexity of the Human CNS versus One View of the Philosophy of Science

15.3 Examples of Unique Individuality: From Pilgrimages to Nature

15.4 Therapeutic Windows for the Treatment of Neurological Diseases

15.4.1 Prevention

15.4.2 Preclinical Treatment

15.4.3 Early-stage, Post-clinical Diagnosis and Treatment

15.4.4 Post-clinical Treatment and its Caveats

16 The Politics and Economics of Neurological Disease

16.1 From the Preface

16.2 The Problems with Single-Hit Models of Neurological Disease

16.3 Summarizing the Main Themes by Chapter

16.4 Can the Amount of Money Spent Change these Outcomes for Neurological Disease Treatment?

16.4.1 Problems of Haecceity and Quiddity

16.4.2 Problems Posed by Biosemiosis (Part 4)

16.5 General Considerations for the Future of Neurological Disease Research

16.6 The Advent of Modern Dentistry and Dental Prophylaxis

16.7 Addressing Neurological Diseases at the Individual and Population Levels

16.7.1 Prophylaxis as a Medical Strategy for Neurological Disease Prevention

16.7.2 The “Politics” of Neurological Disease

16.7.3 The Role of Scientists in the Politics of Neurological Disease Prophylaxis

Glossary

References

Index

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