Key papers in Biological Psychiatry
Pofolia’s corpus holds 50 papers from the Biological Psychiatry subfield (2012–2026). The list below starts with the most cited.
Most cited
Ranked by citation count. Because citations accumulate over time, this list naturally leans towards work published a few years ago; for where the field is now, see “recently added”.
Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies
Cellular Physiology and Biochemistry · 2013 · Q3 · FWCI 161.51 · 8,500 citations · Open access
This review explores the multifaceted molecular mechanisms underlying depression, linking it to metabolic, cardiovascular, endocrine, inflammatory, and neurodegenerative processes.
From stress to inflammation and major depressive disorder: A social signal transduction theory of depression.
Psychological Bulletin · 2014 · Q1 · SJR 8.00 · FWCI 31.42 · 2,177 citations
This review proposes a new theory linking social stress to depression through inflammation, suggesting that social threats activate immune responses, leading to proinflammatory cytokines that drive depressive symptoms.
Microbial tryptophan catabolites in health and disease
Nature Communications · 2018 · Q1 · SJR 4.00 · FWCI 34.03 · 2,147 citations · Open access
Gut microbes produce tryptophan catabolites that influence host health by interacting with the aryl hydrocarbon receptor (AHR), affecting the intestinal barrier, gut hormones, and systemic inflammation.
A Randomized Controlled Trial of the Tumor Necrosis Factor Antagonist Infliximab for Treatment-Resistant Depression
JAMA Psychiatry · 2012 · Q1 · SJR 5.00 · FWCI 22.00 · 1,591 citations
The TNF antagonist infliximab did not show overall efficacy for treatment-resistant depression, but it improved depressive symptoms in patients with high baseline inflammatory biomarkers (hs-CRP > 5 mg/L).
Peripheral cytokine and chemokine alterations in depression: a meta‐analysis of 82 studies
Acta Psychiatrica Scandinavica · 2017 · Q1 · SJR 2.00 · FWCI 33.76 · 1,436 citations
A meta-analysis of 82 studies found that individuals with major depressive disorder (MDD) have significantly elevated levels of several key cytokines and chemokines, including IL-6 and TNF-alpha, compared to healthy controls.
So depression is an inflammatory disease, but where does the inflammation come from?
BMC Medicine · 2013 · Q1 · SJR 2.00 · FWCI 19.29 · 1,411 citations · Open access
This review identifies environmental factors like psychosocial stress, poor diet, and inactivity as potential sources of chronic inflammation that mediate depression risk and progression.
Kynurenines: Tryptophan’s metabolites in exercise, inflammation, and mental health
Science · 2017 · Q1 · SJR 10.00 · FWCI 22.15 · 1,350 citations
Kynurenine metabolites, derived from tryptophan breakdown, are crucial regulators of host-microbiome signaling, immune responses, and neuronal activity. Their accumulation in the brain is linked to depression and schizophrenia, but can be reduced by exercise-induced clearance in skeletal muscle.
Impact of the Gut Microbiota on Intestinal Immunity Mediated by Tryptophan Metabolism
Frontiers in Cellular and Infection Microbiology · 2018 · Q1 · SJR 1.00 · FWCI 30.58 · 1,284 citations · Open access
The gut microbiota significantly influences intestinal immunity by modulating tryptophan (Trp) metabolism, affecting both host and bacterial Trp metabolites. These metabolites, particularly those acting as aryl hydrocarbon receptor (AhR) ligands, are crucial for maintaining immune homeostasis.
Sodium oligomannate therapeutically remodels gut microbiota and suppresses gut bacterial amino acids-shaped neuroinflammation to inhibit Alzheimer’s disease progression
Cell Research · 2019 · Q1 · SJR 6.00 · FWCI 36.82 · 1,134 citations · Open access
Sodium oligomannate (GV-971) reverses Alzheimer's disease (AD) progression by remodeling gut microbiota, reducing specific amino acids (phenylalanine and isoleucine), and suppressing neuroinflammation.
Kynurenine Pathway of Tryptophan Metabolism: Regulatory and Functional Aspects
International Journal of Tryptophan Research · 2017 · Q1 · SJR 1.00 · FWCI 20.59 · 1,131 citations · Open access
The kynurenine pathway (KP) degrades approximately 95% of dietary tryptophan, with the liver handling 90% via TDO and extrahepatic tissues playing a larger role during immune activation via IDO. This pathway produces immunoregulatory and neuroactive metabolites, and its dysregulation is implicated in various diseases.
Cumulative meta-analysis of interleukins 6 and 1β, tumour necrosis factor α and C-reactive protein in patients with major depressive disorder
Brain Behavior and Immunity · 2015 · Q1 · SJR 2.00 · FWCI 5.08 · 1,124 citations
This cumulative meta-analysis confirms higher mean levels of interleukin-6 (IL-6) and C-reactive protein (CRP) in patients with major depressive disorder (MDD) compared to controls, with associations established early in the literature and consistently confirmed.
Neuroinflammation and depression: A review
European Journal of Neuroscience · 2020 · Q2 · FWCI 28.73 · 1,079 citations
Neuroinflammation is increasingly recognized as a central factor in major depressive disorder, interacting with serotonin depletion, HPA axis dysregulation, and altered hippocampal neurogenesis.
Neuroimmune Interactions: From the Brain to the Immune System and Vice Versa
Physiological Reviews · 2017 · Q1 · SJR 11.00 · FWCI 14.66 · 1,052 citations · Open access
This review highlights the crucial, bidirectional communication between the nervous and immune systems, challenging the historical isolation of these fields.
Effect of Anti-inflammatory Treatment on Depression, Depressive Symptoms, and Adverse Effects
JAMA Psychiatry · 2014 · Q1 · SJR 5.00 · FWCI 18.06 · 943 citations
A meta-analysis of 14 trials found that anti-inflammatory treatments, particularly celecoxib, significantly reduced depressive symptoms compared to placebo (SMD -0.34). No increased risk of gastrointestinal, cardiovascular, or infection-related adverse events was observed within 6-12 weeks.
Major depressive disorder: hypothesis, mechanism, prevention and treatment
Signal Transduction and Targeted Therapy · 2024 · Q1 · SJR 17.00 · FWCI 116.24 · 942 citations · Open access
This review comprehensively summarizes the latest research on major depressive disorder (MDD), highlighting the complexity of its pathogenesis and the need for novel diagnostic and therapeutic strategies beyond current single-hypothesis explanations.
Role of neuroinflammation in neurodegenerative diseases (Review)
Molecular Medicine Reports · 2016 · Q2 · FWCI 19.70 · 937 citations · Open access
Neuroinflammation, driven by pro-inflammatory cytokines, is increasingly linked to the pathophysiology of neurodegenerative diseases like Alzheimer's, multiple sclerosis, Parkinson's, and ALS, and their associated depression and dementia.
Role of Translocator Protein Density, a Marker of Neuroinflammation, in the Brain During Major Depressive Episodes
JAMA Psychiatry · 2015 · Q1 · SJR 5.00 · FWCI 25.17 · 928 citations
Major depressive episodes (MDE) are associated with a 26-33% increase in translocator protein density (TSPO VT), a marker of microglial activation, in key brain regions like the prefrontal cortex, anterior cingulate cortex (ACC), and insula.
Inflammatory markers in depression: A meta-analysis of mean differences and variability in 5,166 patients and 5,083 controls
Brain Behavior and Immunity · 2020 · Q1 · SJR 2.00 · FWCI 8.87 · 904 citations
This meta-analysis of 107 studies (5,166 depressed patients, 5,083 controls) confirms depression is a pro-inflammatory state, with significantly elevated levels of key markers like CRP, IL-6, and TNFα.
The Serotonin Theory of Depression: A Systematic Umbrella Review of the Evidence
Molecular Psychiatry · 2022 · Q1 · SJR 4.00 · FWCI 49.31 · 900 citations · Open access
This umbrella review found no consistent evidence supporting the serotonin theory of depression, which posits that depression is caused by lowered serotonin activity or concentrations.
CYTOKINE TARGETS IN THE BRAIN: IMPACT ON NEUROTRANSMITTERS AND NEUROCIRCUITS
Depression and Anxiety · 2013 · Q1 · SJR 1.00 · FWCI 12.13 · 888 citations
Inflammatory cytokines can enter the brain and alter neurotransmitter systems like serotonin, dopamine, and glutamate, impacting neurocircuits involved in mood and behavior.
Recently added
Exercise and the Kynurenine pathway: Current state of knowledge and results from a randomized cross-over study comparing acute effects of endurance and resistance training
PubMed · 2026 · 79 citations
A single bout of endurance exercise, unlike resistance exercise, acutely alters the kynurenine (KYN) pathway in healthy males, increasing kynurenic acid (KA) and quinolinic acid (QA) levels.
Impairments of Neuroplasticity and Cellular Resilience in Severe Mood Disorders: Implications for the Development of Novel Therapeutics
Psychopharmacology Bulletin · 2025 · Q3 · FWCI 1.64 · 329 citations
Severe mood disorders are linked to reduced brain volume and fewer glia/neurons, indicating impaired structural plasticity and cellular resilience, not just neurochemical imbalances.
The Role of GABA in the Pathophysiology and Treatment of Anxiety Disorders
Psychopharmacology Bulletin · 2025 · Q3 · FWCI 4.92 · 266 citations
The GABA system is a central mediator in anxiety disorders, with evidence suggesting a deficiency in GABA neurotransmission contributes to their pathology.
Oxidative stress and inflammation in the pathogenesis of neurological disorders: Mechanisms and implications
Acta Pharmaceutica Sinica B · 2024 · Q1 · SJR 3.00 · FWCI 70.58 · 572 citations
Oxidative stress, an imbalance of reactive oxygen species (ROS), is a key driver in the development of neurological disorders like Alzheimer's, Parkinson's, and stroke.
Major depressive disorder: hypothesis, mechanism, prevention and treatment
Signal Transduction and Targeted Therapy · 2024 · Q1 · SJR 17.00 · FWCI 116.24 · 942 citations · Open access
This review comprehensively summarizes the latest research on major depressive disorder (MDD), highlighting the complexity of its pathogenesis and the need for novel diagnostic and therapeutic strategies beyond current single-hypothesis explanations.
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