Mini reviewEffects of interleukin-1beta polymorphisms on brain function and behavior in healthy and psychiatric disease conditions

- Interleukin-1beta (IL1B) is widely distributed in the brain and has been implicated in the pathogenesis of various psychiatric disorders.
- Several IL1B polymorphisms have been described in relation to various IL1B expression levels in response to inflammatory stimulation.
- Most of the positive-finding studies reported that the IL1B-511T allele is the risk allele for psychiatric diseases or impaired cognition.

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.

80Proposed cascade of pathophysiological mechanisms and events by which Interleukin-1beta polymorphisms may mediate the development of psychiatric disorders.