Effects of interleukin-1beta polymorphisms on brain function and behavior in healthy and psychiatric disease conditions
Abstract
A high level of Interleukin-1beta (IL1B), a key mediator of inflammation, is expressed in the brain, particularly in the hippocampus, which plays a pivotal role in memory and mood regulation. In the brain, IL1B exerts a myriad of effects such as neuronal proliferation, differentiation, apoptosis, and long-term potentiation. Considering its pleiotropic effects in the brain, IL1B has been implicated in the pathogenesis of various psychiatric disorders as well as cognitive function in normal individuals. Thus, IL1B has been considered a candidate gene for the study of psychiatric diseases as well as brain function in normal individuals. The polymorphisms of IL1B have been described in relation to various expression levels in response to stimulation. This review describes previous studies on the genetic effects of IL1B, which relate it to psychiatric diseases such as major depressive disorder, bipolar disorder, schizophrenia, and Alzheimer's disease, as well as cognitive function in normal individuals. Although many reports have indicated a possible role of the genetic effects of IL1B or its phenotypes in psychiatric diseases, some reports were unable to confirm these findings. IL1B release is mediated by an inflammatory response or psychological stress, leading to a cascade of immune reactions involving numerous immune components. To further explore the genetic effects of IL1B on mental diseases and brain function, gene-gene and gene-environment interactions should also be considered.
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IL-1β and IL-18 have essential roles for physiological functions in the CNS, as they participate in processes of cognition, learning, and memory.
“Moreover, IL-1β and IL-18 also have essential roles for physiological functions in the CNS, as they participate in processes of cognition, learning, and memory (201).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [201]
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- Authors
- Tsai, S.-J.
- Affiliations
- Taipei Veterans General Hospital (TW)
- Corresponding author
- Tsai, Shih-Jen
- ORCID
- Tsai, Shih-Jen
- Venue
- Cytokine & Growth Factor Reviews
- Publisher
- Elsevier BV
- Published
- 2017-10
- Volume
- 37
- Pages
- 89-97
- ISSN
- 1359-6101 (ISSN-L)
- OpenAlex
- W2620755913
- Cited by
- 98
- References
- 125
- Citations by year
- 2026: 13 · 2025: 10 · 2024: 12 · 2023: 9 · 2022: 12 · 2021: 9 · 2020: 13 · 2019: 9 · 2018: 7 · 2017: 4
- FWCI
- 0.61
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cytokine & Growth Factor Reviews (publishedVersion)
- PubMed (publishedVersion)
- Funders
- MOST (103-2314-B-075-067-MY3)
- Taiwan Ministry of Science and Technology (V105E17-002-MY2-1, V105C-008, VGHUST103-G1-4-1)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- IL-1β, genetic susceptibility, mental illness, major depressive disorder, bipolar disorder, schizophrenia, Alzheimer's disease, cognitive function, hippocampus, neuroinflammation, psychological stress, gene-environment interaction, gene-gene interaction
- MeSH terms
- Adult, Alleles, Animals, Mental Disorders, Brain, Depressive Disorder, Major, Major Depressive Disorder, Genotype, Humans, Schizophrenia, Mood Disorders, Polymorphism, Single Nucleotide, Interleukin-1beta
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