Clinical and Biochemical Manifestations of Depression: Relation to the Neurobiology of Stress
Open accessAbstract
Major depressive disorder (MDD) is a chronic, recurrent, and severe psychiatric disorder with high mortality and medical comorbidities. Stress-related pathways have been directly involved in the pathophysiology and treatment of MDD. The present paper provides an overview on the stress system as a model to understand key pathophysiological paradigms in MDD. These mechanisms involve behavioral, cognitive, and systemic manifestations and are also associated with the mechanisms of action of effective antidepressants. Aspects such as depression subtypes, inflammation, insulin resistance, oxidative stress, and prothrombotic states in critical brain circuits and periphery are critically appraised. Finally, new strategies for approaching treatment-resistant major depression and potential adverse effects associated with this complex and intricate network are highlighted. The authors used PubMed as the database for this review. Each author extracted relevant data and assessed the methodological quality of each study.
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Hypercortisolism is a relevant feature associated with melancholic-type depression and is present in many people with MDD and in animals subjected to stress.
“Hypercortisolism is one of the relevant mechanisms involved in response to stress and is present in many people with MDD and in animals subjected to stress in the laboratory.”
From Stress and serum cortisol levels in major depressive disorder: a cross-sectional study (2020) · cites this paper as [9]
Section 5.1 associates hypercortisolism with major depression with melancholic features, and Section 2 lists it among signs of melancholia. The copy does not establish that it is present in many people with MDD generally or in laboratory animals subjected to stress; Section 8 discusses heightened stress responses in experimental animals without identifying hypercortisolism. (LLM, conf=0.87)
Experimental — accuracy not yet measuredChronic stress throughout life involves biological changes that underlie MDD in many patients and in laboratory animals.
“Chronic stress throughout life involves several biological changes, which are underlying MDD in many patients and in laboratory animals [4],[6],[9].”
From Stress and serum cortisol levels in major depressive disorder: a cross-sectional study (2020) · cites this paper as [9]
Insulin resistance and inflammation can cause anxiety.
“Insulin resistance and inflammation can cause anxiety [47]”
From The Effect of Anxiety and Nutritional Habits on the Body Distortion of Athletes. (2025) · cites this paper as [47]
Sections 3.3 and 3.4 describe insulin resistance and inflammation as components of the stress response, while Section 8 describes anxiety in the context of depression. None of these passages says that insulin resistance or inflammation causes anxiety; searches for those causal links found no supporting passage in our copy. Page numbers were not available. (LLM, conf=0.74)
Experimental — accuracy not yet measuredExperiential avoidance has been associated with anxiety.
“Experiential avoidance seeks to control the way or frequency of aversive private experiences [37] and has been associated with anxiety [38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54].”
From The Effect of Anxiety and Nutritional Habits on the Body Distortion of Athletes. (2025) · cites this paper as [47]
Section 4.2 discusses aversive emotional memories and fear, and Section 8 discusses anxiety in depression, but neither addresses an association between experiential avoidance and anxiety. Searches for “experiential avoidance” and avoidance of aversive private experiences found no passage making that link; page numbers were not available in our copy. (LLM, conf=0.72)
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“Exposure to stress, which is considered to be a precipitant of depression [79], activates the LC through efferents from the corticotropin-releasing factor (CRF) system [80].”
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“C psychosocial stress represents an increasingly recognized societal burden and a recognized risk factor for the development of numerous mental disorders, including posttraumatic stress disorder (PTSD) (1, 2).”
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“The World Health Organization has classified this disorder as the 4th leading etiology of disability globally (Andrey and Jaime, 2009; Kupfer et al., 2012; Gold et al., 2015).”
BackgroundIs depression the missing link between inflammatory mediators and cancer?
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“Physiologically, experience of reward attenuates with decreased NAc neuronal activity and dopamine release (Gold, 2015).”
BackgroundDepression and substance use disorders: Clinical comorbidity and shared neurobiology
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“The characteristics are severe intensity of symptoms in the first part of the day, awakening insomnia, bradykinesia, significant weight loss with absence of hunger (differential diagnosis with anorexia nervosa in which hunger is present) and feelings of guilt developed and felt in excess [7].”
BackgroundLifestyle Shapes the Dialogue between Environment, Microglia, and Adult Neurogenesis
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“Stress can also trigger depression, as well as influence the length and severity of depressive episodes (Gold et al., 2015).”
BackgroundEvaluation of antidepressant activity of vanillin in mice
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“reflect changes in brain monoamine transmitters, specifically norepinephrine, serotonin, and dopamine.[2] Despite the advent”
BackgroundStress and serum cortisol levels in major depressive disorder: a cross-sectional study
G Bertollo, A., 1 Laboratory of Physiology Pharmacology and Psychopathology, G. P. I. B. S., E Grolli, R., E Plissari, M., A Gasparin, V., Quevedo, J., Z Réus, G., D Bagatini, M., M Ignácio, Z., 2 Santa Catarina State University, W. H. E. C., et al. (2020) · AIMS Neuroscience · doi:10.3934/neuroscience.2020028 · Cited by 56 · see citing works
“Hypercortisolism is a relevant feature associated with melancholic-type depression [9].”
BackgroundInfluentialSex Differences in Depression and Anxiety
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“(gamma-aminobutyric acid) neurotransmissions [2,7,8].”
Chronic psychosocial stress disturbs long-bone growth in adolescent mice
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“Chronic psychosocial stress represents an increasing burden in our modern society and is an accepted risk factor for the development of numerous mental disorders, including post-traumatic stress disorder (PTSD) and depression (Yehuda and Seckl, 2011; Gold et al., 1988).”
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“…are problematic given their ability to dysregulate neurotransmission and trophic factor signaling as well as effectuate decrements in neurogenesis and neuroplasticity (Dantzer et al., 2008; Gold et al., 2015; Khairova et al., 2009; McNally et al., 2008; Miller et al., 2009; Skolnick et al., 2009).”
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“[12] Current depression is clearly linked with alterations of HPA function,[13, 14] including elevated basal cortisol levels and impaired negative feedback inhibition.”
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Depression Following Major Life Transitions in Women: A Review and Theory
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“Although the expression of IL-6 and eotaxin-1 was higher in stressed mice, no statistical significance was observed for any of the genes analyzed, as shown in Supplementary Fig.”
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Skin conductance responses in Major Depressive Disorder (MDD) under mental arithmetic stress
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Social Determinants of Health: An Overview for the Primary Care Provider
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“Poor sleep may be antecedent to depression or co-morbid with depression (Gold et al., 2015; Palagini et al., 2013; Pillai et al., 2011).”
BackgroundNeurochemistry of Neurochemicals: Messengers of Brain Functions
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“Depression [71, 72] Critical aberrations in cholinergic, catecholaminergic (i.”
BackgroundDistinctive stress sensitivity and anxiety-like behavior in female mice: Strain differences matter
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“In stress-related disorders such as melancholic depression, the activities of central glutamate, norepinephrine, central cytokines and pro-inflammatory mediators are significantly and persistently increased (Gold et al., 2015).”
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HPA Axis Interactions with Behavioral Systems
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“[2] The monoamine hypothesis of depression states that it is caused by functional deficit of monoamines (norepinephrine, serotonin and dopamine) at certain sites in the brain.[3] Previously study presented the first evidence for a dopaminergic dysfunction in depression.”
The Effect of Swimming on Anxiety-Like Behaviors and Corticosterone in Stressed and Unstressed Rats
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“Elevated plasma cortisol levels are common in patients with anxiety [40].”
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“Moreover, a growing body of evidence has shown the association between increased levels of biomarkers of oxidative stress and development of depression (Milne et al., 2005; Black et al., 2015; Gold et al., 2015).”
BackgroundMood Therapeutics: Novel Pharmacological Approaches for Treating Depression
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“increased glutamate release, as well as oxidative stress [76,95].”
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“Several psychiatric disorders including depression and schizophrenia have been associated with changes in the stress system and a proinflammatory state of the immune system [Gibney and Drexhage, 2013; Gold et al., 2015].”
BackgroundPathophysiology of Major Depression by Clinical Stages
de Menezes Galvão, A. C., Almeida, R. N., de Sousa, G. M., Leocadio-Miguel, M. A., Palhano-Fontes, F., de Araujo, D. B., Lobão-Soares, B., Maia-de-Oliveira, J. P., Nunes, E. A., Hallak, J. E. C., et al. (2021) · Frontiers in Psychology · doi:10.3389/fpsyg.2021.641779 · Cited by 31 · see citing works
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“Paradoxically, impairments in HPA negative feedback inhibition and subsequent hypercortisolemia, which have been described in studies of major depression [9,10], have not been observed in PTSD patients.”
Background
- Authors
- Gold, P. W., Machado-Vieira, R., & Pavlatou, M. G.
- Affiliations
- National Institutes of Health (US)
- National Institute of Mental Health Intramural Research Program, National Institutes of Health, Bethesda, MD 20892, USA
- Corresponding author
- Gold, Phillip W.
- ORCID
- Pavlatou, Maria G.
- Venue
- Neural Plasticity
- Publisher
- Hindawi Limited
- Published
- 2015
- Volume
- 2015
- Pages
- 1-11
- ISSN
- 1687-5443 (ISSN-L)
- 2090-5904
- PMC
- PMC4387963
- OpenAlex
- W2055457894
- Cited by
- 259
- References
- 53
- Citations by year
- 2026: 12 · 2025: 12 · 2024: 15 · 2023: 17 · 2022: 17 · 2021: 26 · 2020: 24 · 2019: 24 · 2018: 27 · 2017: 29 · 2016: 20 · 2015: 6 · 2014: 3 · 2013: 2 · 2012: 3
- FWCI
- 3.43
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Neural Plasticity (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- major depressive disorder, stress system, neurobiology of stress, depression pathophysiology, antidepressant mechanism, depression subtypes, inflammation, insulin resistance, oxidative stress, hypercoagulability, treatment-resistant depression, antidepressant side effects
- MeSH terms
- Animals, Brain, Depressive Disorder, Homeostasis, Humans, Inflammation, Neuronal Plasticity, Stress, Physiological, Stress, Psychological, Oxidative Stress, Neurogenesis
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