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Inflammation-Associated Depression: Evidence, Mechanisms and Implications

Overview of attention for book
Cover of 'Inflammation-Associated Depression: Evidence, Mechanisms and Implications'

Table of Contents

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    Book Overview
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    Chapter 2 Evidence for Inflammation-Associated Depression
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    Chapter 5 Suicidality and Activation of the Kynurenine Pathway of Tryptophan Metabolism.
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    Chapter 6 Role of the Kynurenine Metabolism Pathway in Inflammation-Induced Depression: Preclinical Approaches.
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    Chapter 7 Depression in Autoimmune Diseases.
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    Chapter 12 Role of Kynurenine Metabolism Pathway Activation in Major Depressive Disorders.
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    Chapter 13 The Role of Dopamine in Inflammation-Associated Depression: Mechanisms and Therapeutic Implications
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    Chapter 14 Role of Inflammation in the Development of Neuropsychiatric Symptom Domains: Evidence and Mechanisms.
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    Chapter 19 Are Non-steroidal Anti-Inflammatory Drugs Clinically Suitable for the Treatment of Symptoms in Depression-Associated Inflammation?
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    Chapter 23 Mechanisms of Inflammation-Associated Depression: Immune Influences on Tryptophan and Phenylalanine Metabolisms.
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    Chapter 25 Stress-Induced Microglia Activation and Monocyte Trafficking to the Brain Underlie the Development of Anxiety and Depression.
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    Chapter 26 The Promise and Limitations of Anti-Inflammatory Agents for the Treatment of Major Depressive Disorder
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    Chapter 28 Inflammation-Associated Co-morbidity Between Depression and Cardiovascular Disease
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    Chapter 30 Brain Structures Implicated in Inflammation-Associated Depression
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    Chapter 31 Does Diet Matter? The Use of Polyunsaturated Fatty Acids (PUFAs) and Other Dietary Supplements in Inflammation-Associated Depression.
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    Chapter 37 Immune-to-Brain Communication Pathways in Inflammation-Associated Sickness and Depression
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    Chapter 40 Inflammation Effects on Brain Glutamate in Depression: Mechanistic Considerations and Treatment Implications.
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    Chapter 43 Role of Neuro-Immunological Factors in the Pathophysiology of Mood Disorders: Implications for Novel Therapeutics for Treatment Resistant Depression.
Attention for Chapter 40: Inflammation Effects on Brain Glutamate in Depression: Mechanistic Considerations and Treatment Implications.
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Chapter title
Inflammation Effects on Brain Glutamate in Depression: Mechanistic Considerations and Treatment Implications.
Chapter number 40
Book title
Inflammation-Associated Depression: Evidence, Mechanisms and Implications
Published in
Current topics in behavioral neurosciences, November 2016
DOI 10.1007/7854_2016_40
Pubmed ID
Book ISBNs
978-3-31-951151-1, 978-3-31-951152-8
Authors

Ebrahim Haroon, Andrew H. Miller, Haroon, Ebrahim, Miller, Andrew H.

Editors

Robert Dantzer, Lucile Capuron

Abstract

There has been increasing interest in the role of glutamate in mood disorders, especially given the profound effect of the glutamate receptor antagonist ketamine in improving depressive symptoms in patients with treatment-resistant depression. One pathway by which glutamate alterations may occur in mood disorders involves inflammation. Increased inflammation has been observed in a significant subgroup of patients with mood disorders, and inflammatory cytokines have been shown to influence glutamate metabolism through effects on astrocytes and microglia. In addition, the administration of the inflammatory cytokine interferon-alpha has been shown to increase brain glutamate in the basal ganglia and dorsal anterior cingulate cortex as measured by magnetic resonance spectroscopy (MRS). Moreover, MRS studies in patients with major depressive disorder have revealed that increased markers of inflammation including C-reactive protein correlate with increased basal ganglia glutamate, which in turn was associated with anhedonia and psychomotor retardation. Finally, human and laboratory animal studies have shown that the response to glutamate antagonists such as ketamine is predicted by increased inflammatory cytokines. Taken together, these data make a strong case that inflammation may influence glutamate metabolism to alter behavior, leading to depressive symptoms including anhedonia and psychomotor slowing.

Mendeley readers

The data shown below were compiled from readership statistics for 81 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 81 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 13 16%
Student > Ph. D. Student 13 16%
Student > Bachelor 10 12%
Student > Master 9 11%
Student > Doctoral Student 6 7%
Other 12 15%
Unknown 18 22%
Readers by discipline Count As %
Neuroscience 16 20%
Medicine and Dentistry 14 17%
Psychology 7 9%
Pharmacology, Toxicology and Pharmaceutical Science 3 4%
Biochemistry, Genetics and Molecular Biology 3 4%
Other 10 12%
Unknown 28 35%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 21 May 2018.
All research outputs
#8,133,704
of 12,968,481 outputs
Outputs from Current topics in behavioral neurosciences
#197
of 339 outputs
Outputs of similar age
#203,218
of 368,559 outputs
Outputs of similar age from Current topics in behavioral neurosciences
#21
of 35 outputs
Altmetric has tracked 12,968,481 research outputs across all sources so far. This one is in the 23rd percentile – i.e., 23% of other outputs scored the same or lower than it.
So far Altmetric has tracked 339 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.0. This one is in the 33rd percentile – i.e., 33% of its peers scored the same or lower than it.
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We're also able to compare this research output to 35 others from the same source and published within six weeks on either side of this one. This one is in the 25th percentile – i.e., 25% of its contemporaries scored the same or lower than it.