‘It's not over when it's over’: persistent neurobiological abnormalities in recovered depressed patients
Open accessAbstract
The tendency of major depression to recur is a leading problem in clinical management and is responsible for much of the illness burden. Until recently, biological studies of depression have focused on the mechanisms involved in acute illness but there are now many data to suggest that neurobiological abnormalities persist when depressed patients are clinically recovered and withdrawn from medication. These abnormalities encompass a number of neurochemical and neuropsychological mechanisms that could be relevant to recurrence, including changes in the availability of serotonin (5-hydroxytryptamine, 5-HT) receptor subtypes, decreases in cortical γ-aminobutyric acid (GABA), increases in cortisol secretion and negative biases in the processing of emotional information. Studies of groups at high risk of depression before illness onset will help to clarify which biological abnormalities precede the development of depression and which are the product of recurrent illness. Ultimately this work should lead to a better understanding of the neurobiology of vulnerability to depression and more innovative approaches to primary and secondary prevention.
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Preventive strategies that identify and ameliorate vulnerability factors could reduce risk of subsequent episodes of major depressive disorder.
“Preventive strategies that identify and ameliorate these factors ostensibly could reduce risk of subsequent episodes [6].”
The continued significant decrease in β2*-nAChR availability in fully recovered, euthymic, medication-free rMDD subjects suggests that the changes in MDD are not an epiphenomenon of treatment or illness but may be associated with trait vulnerability to depression.
“The continued, significant decrease in β2*-nAChR availability in fully recovered, euthymic, medication free rMDD subjects suggests that the changes in MDD are not an epiphenomenon of treatment or illness but may be associated with trait vulnerability to depression as demonstrated by us previously for other targets (26, 41, 42).”
From Persistent β <sub>2</sub> *-Nicotinic Acetylcholinergic Receptor Dysfunction in Major Depressive Disorder (2012) · cites this paper as [26]
It is not yet clearly established whether HPA-axis alterations in MDD are correlates or consequences of depressive disorder/treatments or risk factors present before onset.
“It is not yet clearly established in human populations whether such alterations are correlates or consequences of the experience of depressive disorder and/or its treatments, or whether they reflect risk or vulnerability factors that are present prior to the onset of disorder, thus potentially playing a role in the pathophysiology of MDD (Bhagwagar and Cowen, 2007).”
From Prospective prediction of major depressive disorder from cortisol awakening responses in adolescence (2010) · cites this paper as Bhagwagar and Cowen, 2007
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- Authors
- Bhagwagar, Z., & Cowen, P. J.
- Affiliations
- Yale University (US)
- Warneford Hospital (GB)
- Corresponding author
- Cowen, P.J.
- Venue
- Psychological Medicine
- Publisher
- Cambridge University Press (CUP)
- Published
- 2007-08-03
- Volume
- 38
- Issue
- 3
- Pages
- 307-313
- ISSN
- 0033-2917 (ISSN-L)
- 1469-8978
- OpenAlex
- W2045271226
- Cited by
- 124
- References
- 63
- Citations by year
- 2026: 2 · 2025: 2 · 2022: 5 · 2021: 3 · 2020: 6 · 2019: 5 · 2018: 4 · 2017: 9 · 2016: 5 · 2015: 13 · 2014: 17 · 2013: 8 · 2012: 13
- FWCI
- 0.70
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Psychological Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Eli Lilly and Company
- Medical Research Council
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- major depressive disorder, depression recurrence, remitted depression, serotonin receptor subtypes, GABA, cortisol, depression vulnerability, depression prevention
- MeSH terms
- Acute Disease, Depressive Disorder, Dexamethasone, Electroconvulsive Therapy, gamma-Aminobutyric Acid, Humans, Hydrocortisone, Hypothalamo-Hypophyseal System, Synaptic Transmission, Pituitary-Adrenal System, Recurrence, Saliva, Serotonin, Selective Serotonin Reuptake Inhibitors
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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