Omega-3 Improves cognitive Dysfunction in Schizophrenia Via CREB S133 Phosphorylation Victoria Radburn
Schizophrenia (SZ) is a complex mental health disorder associated with social, behavioural and cognitive impairments. It is found to produce reduced levels of brain-derived neurotrophic factor (BDNF), which is key for learning and memory function. ω-3PUFAs have been shown to increase BDNF levels and improve SZ symptoms through the upregulation for the BDNF/CREB pathway, however the mechanism of action still needs to be understood. Guo, et al. (2020) tested ω3PUFAs on MK801-induced SZ rat models, and found increased BDNF and CREB levels, along with restored hippocampal neuron damage. This led to decreased anxiety, restored cognitive-behavioural functions, such as social ability and spatial memory, increased synaptic plasticity and increased dendritic spine density1. They hypothesized that S133 phosphorylation of CREB was responsible for mediating this beneficial outcome of ω-3PUFA treatment. Using the S133A inactivated CREB mutation, they found decreased BDNF levels and a reduction in cognitive function even when treated with ω-3PUFAs. This indicates the importance of phosphorylated S133 CREB in the pathway to producing improved SZ symptoms. With this understanding, future studies and clinical trials can be implemented to test the efficacy of ω-3PUFAs on humans with SZ. Below is an original visual abstract summary of the Guo, et al. (2020) paper and the results found when treating MK801 rats with ω-3PUFAs
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