Inflammation-associated depression : evidence, mechanisms and implications

Inflammation has invaded the field of psychiatry. The finding that cytokines are elevated in various affective and psychotic disorders brings to the forefront the necessity of identifying the precise research domain criteria (RDoCs) that inflammation is responsible for. This task is certainly the mo...

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Bibliographic Details
Other Authors Dantzer, Robert, Capuron, Lucile
Format Electronic eBook
LanguageEnglish
Published [Place of publication not identified] : Springer, 2017.
SeriesCurrent topics in behavioral neurosciences ; 31.
Subjects
Online AccessFull text
ISBN9783319511528
9783319511511
ISSN1866-3370 ;
Physical Description1 online resource (x, 356 pages) : illustrations

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Table of Contents:
  • Preface; Contents; Evidence for Inflammation-Associated Depression; 1 Introduction; 2 Evidence from Animal Models; 3 Evidence from Clinical Studies; 3.1 Cytokines and Cell-Mediated Immune (CMI) Pathways Contribute to Inflammation and Depression; 3.2 Platelet-Activating Factors (PAFs) and Oxidative and Nitrosative Stress (OandNS) Contribute to Inflammation and Depression; 3.3 Damage to Mitochondria and Mitochondrial DNA Contribute to Inflammation and Depression; 4 Discussion; 5 Conclusion; References.
  • Role of Inflammation in the Development of Neuropsychiatric Symptom Domains: Evidence and Mechanisms1 Inflammation and Neuropsychiatric Symptoms; 1.1 From Sickness to Neuropsychiatric Disorders; 1.2 Towards the Identification of Common Major Symptom Domains Targeted by Inflammatory Processes; 1.3 Evidence for a Role of Inflammation in Distinct Neuropsychiatric Domains; 2 Inflammation and the Specificity of Neuropsychiatric Symptoms Units; 2.1 A Multimodal Biological Substrate; 2.2 Vulnerability and Modulatory Factors; The HPA Axis and Its Relation to Stress; Metabolic Abnormalities.
  • Personality3 Conclusion and Therapeutic Implications; References; Inflammation-Associated Co-morbidity Between Depression and Cardiovascular Disease; 1 Introduction; 2 Epidemiology; 2.1 Depressive Illness; 2.2 Cardiovascular Disease; 2.3 Co-morbidity Between DI and Cardiovascular Disease; 3 Factors Accountable for the Co-morbidity; 3.1 Role of Stress in Inflammation and Depression; 3.2 Autonomic Nervous System Dysfunction; 3.3 Heart Rate Variability; 4 Bidirectionality of Inflammation in Cardiovascular Disease and Depression; 4.1 Inflammation and Depression.
  • 4.2 Inflammation and Cardiovascular Disease4.3 C-Reactive Protein; 4.4 Endothelial Dysfunction; 5 The Tryptophan/Kynurenine Pathway: Implications for Serotonergic Transmission; 6 Inflammation and the Serotonin Transporter; 7 The Glutamatergic Theory of Depression; 8 Other Mechanisms; 9 Treatment Issues; 10 Concluding Remarks; References; Immune-to-Brain Communication Pathways in Inflammation-Associated Sickness and Depression; 1 Periphery-to-Brain Communication Pathways; 1.1 Neural Pathway; 1.2 Signaling via Cerebral Endothelial Cells; 1.3 Signaling via the Circumventricular Organs.
  • 1.4 Peripheral Immune-Cell-to-Brain Signaling2 Changes in Brain Function as a Result of Periphery-to-Brain Communication; 3 Gut Microbiome, Systemic Inflammation, and Altered Behavior and Mood; 3.1 Gut Microbiome and Changes During Inflammatory Diseases; 3.2 Gut-to-Brain Communication Can Modulate Behavior; 3.3 Changes in Gut Microbiome Can Modulate Systemic Inflammation and Thereby Behavior; 3.4 Gut Dysbiosis in Systemic Disease; 4 Concluding Remarks; References; Mechanisms of Inflammation-Associated Depression: Immune Influences on Tryptophan and Phenylalanine Metabolisms; 1 Introduction.