Evidence for a cytokine model of cognitive function

McAfoose, J.; Baune, B.T.

doi:10.1016/j.neubiorev.2008.10.005

Cited by 760Tryptophan and brain disordersNeuroinflammation and Neurodegeneration MechanismsCytokine Signaling Pathways and Interactions

Evidence for a cytokine model of cognitive function

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McAfoose, J., Baune, B.T.·2009·Neuroscience & Biobehavioral Reviews

DOI 10.1016/j.neubiorev.2008.10.005

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Abstract

Aiming at a formulation of a cytokine model of cognitive function under immunologically unchallenged physiological conditions, this article reviews the cytokine biology in the central nervous system (CNS) and recent developments in normal cytokine functions within the CNS that subserve cognitive processes. Currently available evidence shows that the cytokines IL-1beta, IL-6 and TNF-alpha play a role in complex cognitive processes at the molecular level, such as synaptic plasticity, neurogenesis, as well as neuromodulation. Such findings provide evidence for a cytokine model of cognitive function, which shows that cytokines play an intimate role in the molecular and cellular mechanisms subserving learning, memory and cognition under physiological conditions. These cytokine-mediated cognitive processes have implications in the long-term development and pathogenesis of specific neuropsychiatric disorders such as major depression and dementia. The identification of this central role of cytokines in various brain activities during health provides greater insight into normal brain functions, especially synaptic plasticity, memory and cognition, and facilitates the understanding of specific biological mechanisms involved in neuropsychiatric diseases, such as dementia and depression. In order to extend the suggested cytokine model of cognitive function onto other members of the cytokine family, future research is required to investigate the physiological effects of other cytokines such as interferon-gamma (IFNgamma), alpha(1)-antichymotrypsin and IL-2 on cognitive function at the molecular level under immunologically unchallenged conditions.

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Monoamine abnormalities in major depressive disorder likely contribute to impaired cellular signaling and neurocircuit deficits.
“The well-established monoamine abnormalities in MDD likely contribute to impaired cellular signaling and neurocircuit deficits.19”
From Cognitive Impairment in Major Depressive Disorder (2019) · cites this paper as [19]
IL-1beta and IL-6 increase during infection and play central roles in synaptic plasticity, neurogenesis, and neuromodulation.
“IL-1beta and IL-6, both of which increase during infection, have been described as playing a central role in synaptic plasticity, neurogenesis and neuromodulation”
From Glucocorticoids, cytokines and brain abnormalities in depression (2011) · cites this paper as McAfoose and Baune 2009
Under physiological conditions cytokines have a beneficial role on learning and memory, e.g. by promoting long term potentiation (LTP), neural plasticity and neural excitability.
“Under physiological conditions cytokines have a beneficial role on learning and memory, e.g. by promoting long term potentiation (LTP), neural plasticity and neural excitability [3], [52], [53].”
From Dose-dependent effects of endotoxin on neurobehavioral functions in humans (2011) · cites this paper as [52]
Many studies have suggested that inflammation activation is linked to cognitive dysfunction, with a primary role for IL-1β, IL-6, IL-18, and TNF-α.
“Many studies have implied that inflammation activation is inextricably linked to cognitive dysfunction suggesting a primary role of IL-1β, IL-6, IL-18, and TNF-α (Beydoun et al., 2019, Gorelick, 2010, McAfoose and Baune, 2009).”
From Persistent psychopathology and neurocognitive impairment in COVID-19 survivors: effect of inflammatory biomarkers at three-month follow-up (2021) · cites this paper as McAfoose and Baune, 2009
Psychotropic agents may have a similar effect on the immune system and, consequently, on cognitive performance.
“Finally, psychotropic agents may have a similar effect on the immune system and, consequently, on cognitive performance [86, 87].”
From Cognitive remission: a novel objective for the treatment of major depression? (2016) · cites this paper as [86]

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Authors: McAfoose, J., & Baune, B. T.
Affiliations: James Cook University (AU)
Corresponding author: Baune, B.T.
ORCID: Baune, B.T.
Venue: Neuroscience & Biobehavioral Reviews
Publisher: Elsevier BV
Published: 2009-03
Volume: 33
Issue: 3
Pages: 355-366
ISSN: 0149-7634 (ISSN-L)
DOI: 10.1016/j.neubiorev.2008.10.005
OpenAlex: W2168610467
Cited by: 760
References: 198
Citations by year: 2026: 16 · 2025: 32 · 2024: 48 · 2023: 30 · 2022: 45 · 2021: 50 · 2020: 37 · 2019: 59 · 2018: 56 · 2017: 48 · 2016: 57 · 2015: 59 · 2014: 45 · 2013: 52 · 2012: 55
FWCI: 7.91
Type: journal article
Language: en
Open access: green
researchonline.jcu.edu.au
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neuroscience & Biobehavioral Reviews (publishedVersion)
PubMed (publishedVersion)
ResearchOnline - JCU (James Cook University) (submittedVersion)
Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
Topics: Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
Keywords: cytokines, cognitive function, central nervous system, IL-1β, interleukin-6, TNF-α, synaptic plasticity, neurogenesis, neuromodulation, learning and memory, major depressive disorder, dementia, interferon-gamma, alpha-1-antichymotrypsin, interleukin-2
MeSH terms: Animals, Central Nervous System, Cognition, Humans, Memory, Models, Neurological, Neuronal Plasticity, Neurons, Signal Transduction, Cytokines, Neurogenesis

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