ReviewAdvances in experimental medicine and biology2026
Chronic Pain and Major Depression: Shared Psychological and Neurobiological Mechanism.
Review in Advances in experimental medicine and biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- [Mechanistic role of spinal Lamb1 in negative emotionZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Article
- Cognitive Behavioral Therapy and Pain Chronification: Neuroimmune Rationale, Evidence Boundaries, and Trial Design Priorities: A Structured Narrative Review.Journal of pain research · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Depression and chronic pain frequently co-occur, amplifying disease burden and complicating treatment. Shared mechanisms span immune, neurotransmitter, and neuroplastic domains. Neuroinflammation, characterized by elevated cytokines such as IL-6 (interleukin-6) and TNF-α (tumor necrosis factor-alpha), drives both mood dysregulation and nociplastic pain through microglial activation and central sensitization. Dysregulation of glutamate and gamma-aminobutyric acid (GABA) signaling contributes to excitatory-inhibitory imbalance, while altered BDNF (brain-derived neurotrophic factor) expression links neuroplasticity with pain amplification. Substance P and monoamine disturbances further integrate affective and somatic symptoms. Neuroimaging reveals overlapping dysfunction in prefrontal, cingulate, and limbic networks, providing a unifying framework for pain-emotion interactions. Psychological and social factors, including maladaptive cognitions, emotion regulation deficits, and reduced social support, exacerbate this bidirectional relationship. Clinically, tricyclic antidepressants and SNRIs (serotonin-norepinephrine reuptake inhibitors) demonstrate superior analgesic efficacy compared with SSRIs, particularly in neuropathic pain, fibromyalgia, and irritable bowel syndrome. Novel agents such as ketamine and esketamine show rapid antidepressant and potential analgesic effects. Neuromodulation strategies (rTMS (repetitive transcranial magnetic stimulation), tDCS (transcranial direct current stimulation)) and psychological interventions (CBT (cognitive behavioral therapy), mindfulness, ACT (acceptance and commitment therapy)) further enhance outcomes. Together, these findings support a precision medicine approach that integrates biological, psychological, and social determinants. Targeting convergent mechanisms may reduce symptom burden, improve treatment responsiveness, and ultimately enhance quality of life in patients with comorbid depression and chronic pain.
Indexed as
Identifiers
42036566What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.