ReviewActa neuropsychiatrica2025
Immunopsychiatry of late life depression: role of ageing-related immune/inflammatory processes in the development and progression of depression.
Review in Acta neuropsychiatrica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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
7 citing papers in PubMed.
- Neuroinflammatory Mechanisms in Depression: From Biomarkers to Anti-Inflammatory Therapy.Brain sciences · 2026Review
- Comparative analysis of sarcopenic obesity detection and associated mental-cognitive outcomes in community-dwelling older adults: impact of using body mass index versus waist circumference.BMC geriatrics · 2026Article
- Depressive symptoms and functional dependence in near-centenarians and centenarians: a scoping review.BMC geriatrics · 2026Article
- Interplay between Peripheral and Central Nervous System Myeloid Cells during Aging: Impact for Lade-Life Depression and Alzheimer's Disease.Neuroimmunomodulation · 2026Review
- DNA hypomethylation of theFrontiers in neurology · 2026Article
- Response to immune-based augmentation treatment for depression: a potential role of immunosenescence.Neuroscience applied · 2026Article
- Inflammatory and Immune Biomarkers in Mood Disorders: From Mechanistic Pathways to Clinical Translation.Cells · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLate-life depression (LLD) arises from a complex interplay among biological, psychological, and social factors. Biologically, three main hypotheses have been proposed to explain the distinct clinical features of LLD. The vascular hypothesis supports vascular-related white matter changes in the development of LLD, while the neurodegenerative hypothesis suggests that LLD might be a prodrome of neurodegenerative diseases. The inflammatory hypothesis, which is the main focus of this review, posits that heightened inflammation underlies LLD directly or indirectly through neurodegenerative and microvascular alterations.
methodsThis is a non-systematic review on the role played by inflammation in the pathophysiology of LLD and the related opportunities to define biomarkers and therapeutic targets. We searched PubMed from January 2010 through March 2025 for relevant English-language studies.
resultsPatients with LLD have elevated circulating levels of inflammatory biomarkers (e.g., C-reactive protein and interleukin-6) as well as evidence of neuroinflammation. Although the exact origin of this inflammatory profile remains unclear, it is thought to be exacerbated by immune cell senescence and the presence of physical comorbidities, including cardiovascular and metabolic diseases. Pharmacological (e.g., selective serotonin receptor inhibitors) and non-pharmacological (e.g., diet, physical interventions) approaches for LLD seem to exert their therapeutic effect, at least in part, through inflammation-related mechanisms.
conclusionRecognizing the unique features of LLD compared to depression in other periods of life is an important step toward its proper management. More specifically, understanding the role of inflammation in LLD holds both theoretical and practical implications, including anti-inflammatory or immune-based strategies as potential therapeutic interventions.
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