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Inflammation and Its Discontents: The Role of Cytokines in the Pathophysiology of Major Depression
TLDR
Preliminary data from patients with inflammatory disorders, as well as medically healthy depressed patients, suggest that inhibiting proinflammatory cytokines or their signaling pathways may improve depressed mood and increase treatment response to conventional antidepressant medication. Expand
Cytokines sing the blues: inflammation and the pathogenesis of depression.
TLDR
These findings suggest that targeting proinflammatory cytokines and their signaling pathways might represent a novel strategy to treat depression. Expand
The link between childhood trauma and depression: Insights from HPA axis studies in humans
TLDR
Results from a series of clinical studies suggesting that childhood trauma in humans is associated with sensitization of the neuroendocrine stress response, glucocorticoid resistance, increased central corticotropin-releasing factor activity, immune activation, and reduced hippocampal volume are summarized, indicating the existence of biologically distinguishable subtypes of depression as a function of childhood trauma. Expand
A randomized controlled trial of the tumor necrosis factor antagonist infliximab for treatment-resistant depression: the role of baseline inflammatory biomarkers.
TLDR
This proof-of-concept study suggests that TNF antagonism does not have generalized efficacy in treatment-resistant depression but may improve depressive symptoms in patients with high baseline inflammatory biomarkers. Expand
The role of inflammation in depression: from evolutionary imperative to modern treatment target
TLDR
Current understanding of the mechanisms by which the innate and adaptive immune systems interact with neurotransmitters and neurocircuits to influence the risk for depression are detailed. Expand
Glucocorticoid receptors in major depression: relevance to pathophysiology and treatment
TLDR
The data support the hypothesis that the function of the GR is reduced in major depression in the absence of clear evidence of decreased GR expression and indicate that some antidepressants have direct effects on the GR, leading to enhanced GR function and increased GR expression. Expand
Immune system to brain signaling: neuropsychopharmacological implications.
TLDR
The elucidation of the mechanisms by which the immune system influences behavior yields a host of targets for potential therapeutic development as well as informing strategies for the prevention of neuropsychiatric disease in at risk populations. Expand
When not enough is too much: the role of insufficient glucocorticoid signaling in the pathophysiology of stress-related disorders.
TLDR
Neuroendocrine data provide evidence of insufficient glucocorticoid signaling in stress-related neuropsychiatric disorders, including posttraumatic stress disorder and major depression, which are associated with immune system activation/inflammation, high SNS tone, and CRH hypersecretion. Expand
The role of adrenocorticoids as modulators of immune function in health and disease: neural, endocrine and immune interactions
TLDR
This work presents a meta-anatomy of the adrenal gland and its role in the development and management of disease and urges further investigation into the role of “cell reprograming” and “reconcretization” in the course of disease progression. Expand
CSF Concentrations of Brain Tryptophan and Kynurenines during Immune Stimulation with IFN-alpha: Relationship to CNS Immune Responses and Depression
TLDR
Peripheral administration of IFN-α activated IDO in concert with central cytokine responses, resulting in increased brain KYN and QUIN, which correlated with depressive symptoms. Expand
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