HPA axis in major depression: cortisol, clinical symptomatology and genetic variation predict cognition
Open accessAbstract
The hypothalamic-pituitary-adrenal (HPA) axis has been implicated in the pathophysiology of a variety of mood and cognitive disorders. Neuroendocrine studies have demonstrated HPA axis overactivity in major depression, a relationship of HPA axis activity to cognitive performance and a potential role of HPA axis genetic variation in cognition. The present study investigated the simultaneous roles HPA axis activity, clinical symptomatology and HPA genetic variation play in cognitive performance. Patients with major depression with psychotic major depression (PMD) and with nonpsychotic major depression (NPMD) and healthy controls (HC) were studied. All participants underwent a diagnostic interview and psychiatric ratings, a comprehensive neuropsychological battery, overnight hourly blood sampling for cortisol and genetic assessment. Cognitive performance differed as a function of depression subtype. Across all subjects, cognitive performance was negatively correlated with higher cortisol, and PMD patients had higher cortisol than did NPMDs and HCs. Cortisol, clinical symptoms and variation in genes, NR3C1 (glucocorticoid receptor; GR) and NR3C2 (mineralocorticoid receptor; MR) that encode for GRs and MRs, predicted cognitive performance. Beyond the effects of cortisol, demographics and clinical symptoms, NR3C1 variation predicted attention and working memory, whereas NR3C2 polymorphisms predicted memory performance. These findings parallel the distribution of GR and MR in primate brain and their putative roles in specific cognitive tasks. HPA axis genetic variation and activity were important predictors of cognition across the entire sample of depressed subjects and HR. GR and MR genetic variation predicted unique cognitive functions, beyond the influence of cortisol and clinical symptoms. GR genetic variation was implicated in attention and working memory, whereas MR was implicated in verbal memory.
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In some MDD patients, stress leads to long-term elevated glucocorticoids, resulting in synaptic structural changes and remodeling, and stress-induced hyperactivity of the HPA axis leads to negative feedback imbalance of the HPA axis, which is related to depression.
“In some MDD patients, stress leads to long-term elevated glucocorticoids, resulting in synaptic structural changes and remodeling, and the stress-induced hyperactivity of the HPA axis leads to negative feedback imbalance of the HPA axis, which is also related to depression. 39”
From Major depressive disorder: hypothesis, mechanism, prevention and treatment (2024) · cites this paper as [39]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredMediators released by activated microglia can stimulate the HPA axis and induce GC production.
“Mediators released by activated microglia can stimulate the HPA axis and induce GC production. 39”
From Major depressive disorder: hypothesis, mechanism, prevention and treatment (2024) · cites this paper as [39]
The Introduction states that the HPA axis regulates glucocorticoid production. It does not say that mediators released by activated microglia stimulate the axis, so the claimed trigger is unsupported by this paper. (LLM, conf=0.84)
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- Authors
- Keller, J., Gomez, R., Williams, G., Lembke, A., Lazzeroni, L., Murphy, G. M., & Schatzberg, A. F.
- Affiliations
- Stanford Medicine (US)
- Palo Alto University (US)
- Brigham and Women's Hospital (US)
- Corresponding author
- Keller, J
- Venue
- Molecular Psychiatry
- Published
- 2016-08-16
- Volume
- 22
- Issue
- 4
- Pages
- 527-536
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC5313380
- OpenAlex
- W2512630553
- Cited by
- 922
- References
- 61
- Citations by year
- 2026: 113 · 2025: 157 · 2024: 135 · 2023: 125 · 2022: 118 · 2021: 92 · 2020: 82 · 2019: 61 · 2018: 27 · 2017: 10 · 2016: 1
- FWCI
- 21.09
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- National Institutes of Health (UL1TR001085)
- National Institute of Mental Health (R01MH050604, T32MH019938)
- National Center for Research Resources (UL1RR025744)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- major depressive disorder, hypothalamic-pituitary-adrenal axis, cortisol, cognitive performance, glucocorticoid receptor, mineralocorticoid receptor, NR3C1, genetic polymorphism, psychotic depression, attention, working memory, verbal memory, neuroendocrine stress response
- MeSH terms
- Adult, Bipolar Disorder, Brain, Cognition, Cognition Disorders, Major Depressive Disorder, Female, Humans, Hydrocortisone, Hypothalamo-Hypophyseal System, Male, Middle Aged, Pituitary-Adrenal System, Psychotic Disorders, Receptors, Glucocorticoid, Genetic Variation, Receptors, Mineralocorticoid, Polymorphism, Single Nucleotide
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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