ArticleTranslational psychiatry2022
No increase in inflammation in late-life major depression screened to exclude physical illness.
Article in Translational psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Stressful life events and lifestyle factors are associated with elevated peripheral TNF-α levels in adults with depression without physical diseases.European archives of psychiatry and clinical neuroscience · 2026Article
- Comprehensive analysis of cytokines in depression: independent data from patient plasma and post-mortem ventromedial prefrontal cortex.Brain, behavior, & immunity - health · 2026Article
- Remission is insufficient: predictors and mechanistic models of recurrence in late-life depression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Review
- Serum inflammatory cytokines in the progression of depression.Frontiers in immunology · 2026Review
- Intestinal Permeability and Depression-A Narrative Review of Selected Blood-Based Biomarkers.International journal of molecular sciences · 2025Review
- Inflammatory and MRI perfusion biomarkers in predicting persistence of depression: a 6-month Longitudinal Study.Translational psychiatry · 2025Article
- The role of plasma inflammatory markers in late-life depression and conversion to dementia: a 3-year follow-up study.Molecular psychiatry · 2025Article
- The Role of Inflammation in Depression and Beyond: A Primer for Clinicians.Current psychiatry reports · 2024Review
- Neurodevelopmental and Neuropsychiatric Disorders.Advances in neurobiology · 2024Review
- The heterogeneity of late-life depression and its pathobiology: a brain network dysfunction disorder.Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
- Inverse association of anti-inflammatory prescription fills and suicide-related mortality in young adults: Evidence from a nationwide study of Swedish regions, 2006-2021.Brain, behavior, & immunity - health · 2023Article
- Biological factors influencing depression in later life: role of aging processes and treatment implications.Translational psychiatry · 2023Review
- Involvement of inflammatory responses in the brain to the onset of major depressive disorder due to stress exposure.Frontiers in aging neuroscience · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Depression is a common and debilitating disorder in the elderly. Late-life depression (LLD) has been associated with inflammation and elevated levels of proinflammatory cytokines including interleukin (IL)-1β, tumor necrosis factor-alpha, and IL-6, but often depressed individuals have comorbid medical conditions that are associated with immune dysregulation. To determine whether depression has an association with inflammation independent of medical illness, 1120 adults were screened to identify individuals who had clinically significant depression but not medical conditions associated with systemic inflammation. In total, 66 patients with LLD screened to exclude medical conditions associated with inflammation were studied in detail along with 26 age-matched controls (HC). At baseline, circulating cytokines were low and similar in LLD and HC individuals. Furthermore, cytokines did not change significantly after treatment with either an antidepressant (escitalopram 20 mg/day) or an antidepressant plus a COX-2 inhibitor or placebo, even though depression scores improved in the non-placebo treatment arms. An analysis of cerebrospinal fluid in a subset of individuals for IL-1β using an ultrasensitive digital enzyme-linked immunosorbent assay revealed low levels in both LLD and HC at baseline. Our results indicate that depression by itself does not result in systemic or intrathecal elevations in cytokines and that celecoxib does not appear to have an adjunctive antidepressant role in older patients who do not have medical reasons for having inflammation. The negative finding for increased inflammation and the lack of a treatment effect for celecoxib in this carefully screened depressed population taken together with multiple positive results for inflammation in previous studies that did not screen out physical illness support a precision medicine approach to the treatment of depression that takes the medical causes for inflammation into account.
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