Mood disorders, are highly complex conditions influenced by a multitude of factors. These disorders arise from an intricate interlay between genetic predispositions, environmental influences, and neurobiological changes. Genetic risk factors contribute significantly to the susceptibility of developing mood disorders, with certain gene variants linked to the regulation of mood, stress response, and neuroinflammatory processes. Chronic low-grade inflammation has also been increasingly recognized as a key factor, with elevated inflammatory markers such as cytokines and CRP being associated with both the onset and severity of these disroders. Lastly, numerous neuroimaging studies have further highlighted that structural and functional alterations in brain regions involved in emotion regulation, such as the prefrontal cortex and limbic system, are common in individuals with mood disorders. Comprehensively, these genetic, inflammatory, and neuroimaging factors provide a better understanding of the pathophysiology of mood disorders.
In this project, we will use blood-based systemic inflammation markers (e.g., blood CRP levels, Neutrophil-Lymphocyte Ratio) and calculate polygenic risk scores (PRS) following the protocol of prior research (Li C et al., 2024, Brain Behav Immun). Additionally, using the T1 and DTI data, atlas-based cortical thickness, fractional anisotropy (FA), and white matter tractography values will be collected using the UK Biobank’s MRI image processing pipeline. Our a priori hypothesis is that the combination of genetic, inflammatory, and neuroimaging markers will increase the accuracy of distinguishing mood disorders.
