Cognitive Dysfunction in Depression – Pathophysiology and Novel Targets

Carvalho, Andre; Miskowiak, Kamilla; Hyphantis, Thomas; Kohler, Cristiano; Alves, Gilberto; Bortolato, Beatrice; G. Sales, Paulo; Machado-Vieira, Rodrigo; Berk, Michael; McIntyre, Roger

doi:10.2174/1871527313666141130203627

Cited by 107Treatment of Major DepressionTryptophan and brain disordersSchizophrenia research and treatment

Cognitive Dysfunction in Depression – Pathophysiology and Novel Targets

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Carvalho, Andre, Miskowiak, Kamilla, Hyphantis, Thomas, Kohler, Cristiano, Alves, Gilberto, Bortolato, Beatrice, G. Sales, Paulo, Machado-Vieira, Rodrigo +2 more·2015·CNS & Neurological Disorders - Drug Targets

DOI 10.2174/1871527313666141130203627

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Abstract

Major depressive disorder (MDD) is associated with cognitive dysfunction encompassing several domains, including memory, executive function, processing speed and attention. Cognitive deficits persist in a significant proportion of patients even in remission, compromising psychosocial functioning and workforce performance. While monoaminergic antidepressants may improve cognitive performance in MDD, most antidepressants have limited clinical efficacy. The overarching aims of this review were: (1) to synthesize extant literature on putative biological pathways related to cognitive dysfunction in MDD and (2) to review novel neurotherapeutic targets for cognitive enhancement in MDD. We found that reciprocal and overlapping biological pathways may contribute to cognitive dysfunction in MDD, including an hyperactive hypothalamic-pituitary-adrenal axis, an increase in oxidative and nitrosative stress, inflammation (e.g., enhanced production of pro-inflammatory cytokines), mitochondrial dysfunction, increased apoptosis as well as a diminished neurotrophic support. Several promising neurotherapeutic targets were identified such as minocycline, statins, anti-inflammatory compounds, N-acetylcysteine, omega-3 poliunsaturated fatty acids, erythropoietin, thiazolidinediones, glucagon-like peptide-1 analogues, S-adenosyl-l-methionine (SAMe), cocoa flavonols, creatine monohydrate and lithium. Erythropoietin and SAMe had pro-cognitive effects in randomized controlled trials (RCT) involving MDD patients. Despite having preclinical and/or preliminary evidences from trials suggesting possible efficacy as novel cognitive enhancing agents for MDD, no RCT to date was performed for most of the other therapeutic targets reviewed herein. In conclusion, multiple biological pathways are involved in cognitive dysfunction in MDD. RCTs testing genuinely novel pro-cognitive compounds for MDD are warranted.

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A significant proportion of patients with major depressive disorder do not recover baseline levels of psychosocial functioning even when they meet the conventional definition of remission.
“In addition, a significant proportion of patients with MDD do not recover baseline levels of psychosocial functioning even when they meet the conventional definition of remission (e.g. a score ≤7 on the Hamilton Depression Rating Scale (HDRS)) [2, 11, 12], suggesting that non-affective dimensions and domains are critical determinants of functional outcome.”
From Cognitive remission: a novel objective for the treatment of major depression? (2016) · cites this paper as [11]
Many patients with major depressive disorder do not reach premorbid levels of psychosocial functioning, such that a significant proportion present residual symptoms.
“Only a subset of individuals with MDD (30–40 %) reach symptomatic remission after adequate treatment with a first-line antidepressant, and many patients do not reach premorbid levels of psychosocial functioning, such that a significant proportion of patients present residual symptoms.”
From Cognitive remission: a novel objective for the treatment of major depression? (2016) · cites this paper as [11]
Several mechanisms may contribute to cognitive dysfunction in major depressive disorder, including over-activation of the hypothalamic-pituitary-adrenal axis, oxidative and nitrosative stress, imbalances in pathways involved in cell survival and death, and immune activation.
“Several mechanisms may contribute to cognitive dysfunction in MDD, including but not limited to an over-activation of the hypothalamic–pituitary–adrenal axis, oxidative and nitrosative stress, imbalances in pathways involved in cell survival and death, and immune activation [11].”
From Cognitive remission: a novel objective for the treatment of major depression? (2016) · cites this paper as [11]

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“XO is increased in the CNS of patients with MDD; antidepressants decrease XO [124, 125].”
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Authors: Carvalho, A., Miskowiak, K., Hyphantis, T., Kohler, C., Alves, G., Bortolato, B., G. Sales, P., Machado-Vieira, R., Berk, M., & McIntyre, R.
Affiliations: Universidade Federal do Ceará (BR)
Corresponding author: McIntyre, Roger
ORCID: Carvalho, Andre
Miskowiak, Kamilla
Hyphantis, Thomas
Alves, Gilberto
McIntyre, Roger
Venue: CNS & Neurological Disorders - Drug Targets
Publisher: Bentham Science Publishers Ltd.
Published: 2015-01-22
Volume: 13
Issue: 10
Pages: 1819-1835
ISSN: 1568-007X (ISSN-L)
1871-5273
DOI: 10.2174/1871527313666141130203627
OpenAlex: W2150071717
Cited by: 107
References: 252
Citations by year: 2026: 3 · 2025: 5 · 2024: 10 · 2023: 7 · 2022: 12 · 2021: 13 · 2020: 4 · 2019: 9 · 2018: 12 · 2017: 9 · 2016: 17 · 2015: 6
FWCI: 10.62
Type: journal article
Language: en
Open access: green
figshare.com
Licence: cc-by
Locations: CNS & Neurological Disorders - Drug Targets (publishedVersion)
PubMed (publishedVersion)
Deakin Research Online (Deakin University) (submittedVersion)
Figshare (submittedVersion, cc-by)
Topics: Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
Keywords: major depressive disorder, cognitive impairment, cognitive enhancement, hypothalamic-pituitary-adrenal axis, oxidative stress, nitrosative stress, neuroinflammation, inflammatory cytokines, mitochondrial dysfunction, apoptosis, neurotrophic support, minocycline, statins, N-acetylcysteine, omega-3 polyunsaturated fatty acids, erythropoietin, S-adenosylmethionine, creatine monohydrate, lithium, thiazolidinediones, glucagon-like peptide-1 analogues
MeSH terms: Cognition Disorders, Depression, Humans, Nootropic Agents

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Cognitive Dysfunction in Depression – Pathophysiology and Novel Targets

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